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February 27, 2007

(((prostate cancer treatment) AND "2005/11/13 17.56"[MHDA]:"2115/11/20 14.01"[MHDA])) NOT (( (((prostate cancer[TIAB] AND treatment[TIAB]))) AND "0001"[EDAT]:"2005/11/13 17.56"[EDAT])); +1986 new citations


(((prostate cancer treatment) AND "2005/11/13 17.56"[MHDA]:"2115/11/20 14.01"[MHDA])) NOT (( (((prostate cancer[TIAB] AND treatment[TIAB]))) AND "0001"[EDAT]:"2005/11/13 17.56"[EDAT])); +1986 new citations

1986 new PubMed citations were retrieved for your search. Click on the search hyperlink below to display the complete search results:

(((prostate cancer treatment) AND "2005/11/13 17.56"[MHDA]:"2115/11/20 14.01"[MHDA])) NOT (( (((prostate cancer[TIAB] AND treatment[TIAB]))) AND "0001"[EDAT]:"2005/11/13 17.56"[EDAT]))

These PubMed results were generated on 2007/02/27

PubMed, a service of the National Library of Medicine, includes over 15 million citations for biomedical articles back to the 1950's. These citations are from MEDLINE and additional life science journals. PubMed includes links to many sites providing full text articles and other related resources.


Posted by at 8:13 AM |

August 21, 2006

Re: luteinizing hormone-releasing hormone agonist effects on skeletal muscle: how hormonal therapy in prostate cancer affects muscular strength.


Re: luteinizing hormone-releasing hormone agonist effects on skeletal muscle: how hormonal therapy in prostate cancer affects muscular strength.
Related Articles

Re: luteinizing hormone-releasing hormone agonist effects on skeletal muscle: how hormonal therapy in prostate cancer affects muscular strength.

J Urol. 2005 Nov;174(5):2068-9

Authors: Marcora S, Oliver S, Callow N, Lemmey A, Stuart N

PMID: 16217402 [PubMed - indexed for MEDLINE]


Posted by at 4:51 PM |

(((prostate cancer treatment) AND "2005/11/13 17.56"[MHDA]:"2115/11/20 14.01"[MHDA])) NOT (( (((prostate cancer[TIAB] AND treatment[TIAB]))) AND "0001"[EDAT]:"2005/11/13 17.56"[EDAT])); +128 new citations


(((prostate cancer treatment) AND "2005/11/13 17.56"[MHDA]:"2115/11/20 14.01"[MHDA])) NOT (( (((prostate cancer[TIAB] AND treatment[TIAB]))) AND "0001"[EDAT]:"2005/11/13 17.56"[EDAT])); +128 new citations

128 new PubMed citations were retrieved for your search. Click on the search hyperlink below to display the complete search results:

(((prostate cancer treatment) AND "2005/11/13 17.56"[MHDA]:"2115/11/20 14.01"[MHDA])) NOT (( (((prostate cancer[TIAB] AND treatment[TIAB]))) AND "0001"[EDAT]:"2005/11/13 17.56"[EDAT]))

These PubMed results were generated on 2006/08/21

PubMed, a service of the National Library of Medicine, includes over 15 million citations for biomedical articles back to the 1950's. These citations are from MEDLINE and additional life science journals. PubMed includes links to many sites providing full text articles and other related resources.


Posted by at 4:51 PM |

August 9, 2006

Inactivation of Id-1 in prostate cancer cells: A potential therapeutic target in inducing chemosensitization to taxol through activation of JNK pathway.


Inactivation of Id-1 in prostate cancer cells: A potential therapeutic target in inducing chemosensitization to taxol through activation of JNK pathway.
Related Articles

Inactivation of Id-1 in prostate cancer cells: A potential therapeutic target in inducing chemosensitization to taxol through activation of JNK pathway.

Int J Cancer. 2006 Apr 15;118(8):2072-81

Authors: Zhang X, Ling MT, Wang X, Wong YC

Resistance to anticancer drugs is the major problem in the treatment of many advanced cancers, including androgen-independent prostate cancer. Recently, increased expression of Id-1, a basic helix-loop-helix protein, is reported in several types of advanced cancer. It is suggested that high expression of Id-1 may provide an advantage for cancer cell survival and inactivation of Id-1 may be able to increase cancer cells' susceptibility to apoptosis. To test this hypothesis, in this study, by using RNA interfering technology, we inactivated the Id-1 gene in 2 androgen-independent prostate cancer cell lines, DU145 and PC3, and investigated whether downregulation of Id-1 could lead to increased sensitivity to a commonly used anticancer drug, taxol. By using colony forming assay and MTT assay, we found that inactivation of Id-1 resulted in both decreased colony forming ability and cell viability in prostate cancer cells, after taxol treatment. In addition, the si-Id-1-induced sensitization to taxol was associated with activation of apoptosis pathway, which is demonstrated by increased apoptotic index, DNA laddering, sub-G1 phase of the cell cycle, as well as cleaved-PARP and Caspase 3. Furthermore, c-Jun N-terminal kinase (JNK), one of the common pathways responsible for taxol-induced apoptosis, was also activated in the si-Id-1 transfected cells. Inhibition of JNK activity by a specific inhibitor, SP600125, blocked the si-Id-1-induced sensitivity to taxol. These results indicate that increased Id-1 expression in prostate cancer cells may play a protective role against apoptosis, and downregulation of Id-1 may be a potential target to increase sensitivity of taxol-induced apoptosis in prostate cancer cells.

PMID: 16287090 [PubMed - indexed for MEDLINE]


Posted by at 12:42 PM |

(((prostate cancer treatment) AND "2005/11/13 17.56"[MHDA]:"2115/11/20 14.01"[MHDA])) NOT (( (((prostate cancer[TIAB] AND treatment[TIAB]))) AND "0001"[EDAT]:"2005/11/13 17.56"[EDAT])); +634 new citations


(((prostate cancer treatment) AND "2005/11/13 17.56"[MHDA]:"2115/11/20 14.01"[MHDA])) NOT (( (((prostate cancer[TIAB] AND treatment[TIAB]))) AND "0001"[EDAT]:"2005/11/13 17.56"[EDAT])); +634 new citations

634 new PubMed citations were retrieved for your search. Click on the search hyperlink below to display the complete search results:

(((prostate cancer treatment) AND "2005/11/13 17.56"[MHDA]:"2115/11/20 14.01"[MHDA])) NOT (( (((prostate cancer[TIAB] AND treatment[TIAB]))) AND "0001"[EDAT]:"2005/11/13 17.56"[EDAT]))

These PubMed results were generated on 2006/08/09

PubMed, a service of the National Library of Medicine, includes over 15 million citations for biomedical articles back to the 1950's. These citations are from MEDLINE and additional life science journals. PubMed includes links to many sites providing full text articles and other related resources.


Posted by at 12:42 PM |

June 13, 2006

A tumour stem cell hypothesis for the origins of prostate cancer.


A tumour stem cell hypothesis for the origins of prostate cancer.
Related Articles

A tumour stem cell hypothesis for the origins of prostate cancer.

BJU Int. 2005 Dec;96(9):1219-23

Authors: Maitland NJ, Collins A

Cancer stem cells undoubtedly exist in many tumour types, including the prostate. This hypothesis can explain both the heterogeneity of prostate tumours and their variable responses to several conventional therapies. In the longer term, therapies directed against tumour stem cells should offer a real possibility of long-term cure, rather than current palliative therapy. Identifying specific tumour stem-cell markers will enhance this process, but the scarcity of these cells within the mass of more differentiated amplifying progeny that comprise >99.9% of most cancers makes this a severe technical challenge. In addition, many tumour stem-cell markers are probably shared with normal stem cells, both in prostate and in stem cells from other tissues, but tumour-specific patterns of gene expression, probably designed to allow the tumour stem cell to survive outside its protective 'niche' in normal tissues, will be the best initial targets for new therapeutic agents.

PMID: 16287434 [PubMed - indexed for MEDLINE]


Posted by at 8:56 PM |

(((prostate cancer treatment) AND "2005/11/13 17.56"[MHDA]:"2115/11/20 14.01"[MHDA])) NOT (( (((prostate cancer[TIAB] AND treatment[TIAB]))) AND "0001"[EDAT]:"2005/11/13 17.56"[EDAT])); +215 new citations


(((prostate cancer treatment) AND "2005/11/13 17.56"[MHDA]:"2115/11/20 14.01"[MHDA])) NOT (( (((prostate cancer[TIAB] AND treatment[TIAB]))) AND "0001"[EDAT]:"2005/11/13 17.56"[EDAT])); +215 new citations

215 new PubMed citations were retrieved for your search. Click on the search hyperlink below to display the complete search results:

(((prostate cancer treatment) AND "2005/11/13 17.56"[MHDA]:"2115/11/20 14.01"[MHDA])) NOT (( (((prostate cancer[TIAB] AND treatment[TIAB]))) AND "0001"[EDAT]:"2005/11/13 17.56"[EDAT]))

These PubMed results were generated on 2006/06/13

PubMed, a service of the National Library of Medicine, includes over 15 million citations for biomedical articles back to the 1950's. These citations are from MEDLINE and additional life science journals. PubMed includes links to many sites providing full text articles and other related resources.


Posted by at 8:56 PM |

May 24, 2006

Effects of long-term finasteride treatment on prostate cancer morphology and clinical outcome.


Effects of long-term finasteride treatment on prostate cancer morphology and clinical outcome.
Related Articles

Effects of long-term finasteride treatment on prostate cancer morphology and clinical outcome.

Urology. 2005 Nov;66(5):930-4

Authors: Rubin MA, Allory Y, Molinié V, Leroy X, Faucon H, Vacherot F, Huang W, Kuten A, Salomon L, Rebillard X, Cussenot O, Abbou C, de la Taille A

OBJECTIVES: To examine the morphologic alterations of finasteride therapy on prostate cancer compared with no treatment or treatment with a luteinizing hormone-releasing hormone (LHRH) agonist and the clinical outcomes of patients treated with finasteride. METHODS: The data of 56 patients with prostate cancer who had taken finasteride for at least 6 months were reviewed. A central pathology review was performed in a blinded manner comparing these patients with 56 matched controls and 44 patients who received a 3-month course of LHRH agonist before radical prostatectomy. The histologic hormonal treatment effects included apoptosis, vacuolated cytoplasm, pyknotic nuclei, and small irregular glands. An overall consensus was scored using a three-tiered system: no apparent effect (score = 0), suspicious for hormonal effect (score = 1), and highly suggestive of hormonal treatment (score = 2). A Gleason score was assigned to all prostatectomy specimens. RESULTS: The mean hormonal treatment score for the prostatectomy specimens was 0.4, 0.5, and 1.6 for the control, finasteride, and 3-month LHRH groups, respectively. Surprisingly, 20% of control patients had suspicious or highly suggestive hormonal effects and 26% of the finasteride-treated patients did so. For the LHRH-treated group, only 23% did not demonstrate classic features of hormonal treatment. Similar clinical outcomes were observed between the finasteride and control groups. CONCLUSIONS: No consistent hormonal therapy effects with finasteride treatment were observed compared with LHRH agonists. The hormonal effect was observed in the control group. Therefore, although other aspects of the Prostate Cancer Prevention Trial design might account for the greater percentage of Gleason grade tumors in the study arm, morphologic changes due to long-term finasteride treatment were not a likely cause.

PMID: 16286097 [PubMed - indexed for MEDLINE]


Posted by at 10:52 AM |

(((prostate cancer treatment) AND "2005/11/13 17.56"[MHDA]:"2115/11/20 14.01"[MHDA])) NOT (( (((prostate cancer[TIAB] AND treatment[TIAB]))) AND "0001"[EDAT]:"2005/11/13 17.56"[EDAT])); +259 new citations


(((prostate cancer treatment) AND "2005/11/13 17.56"[MHDA]:"2115/11/20 14.01"[MHDA])) NOT (( (((prostate cancer[TIAB] AND treatment[TIAB]))) AND "0001"[EDAT]:"2005/11/13 17.56"[EDAT])); +259 new citations

259 new PubMed citations were retrieved for your search. Click on the search hyperlink below to display the complete search results:

(((prostate cancer treatment) AND "2005/11/13 17.56"[MHDA]:"2115/11/20 14.01"[MHDA])) NOT (( (((prostate cancer[TIAB] AND treatment[TIAB]))) AND "0001"[EDAT]:"2005/11/13 17.56"[EDAT]))

These PubMed results were generated on 2006/05/24

PubMed, a service of the National Library of Medicine, includes over 15 million citations for biomedical articles back to the 1950's. These citations are from MEDLINE and additional life science journals. PubMed includes links to many sites providing full text articles and other related resources.


Posted by at 10:52 AM |

May 21, 2006

Is dehydroepiandrosterone a hormone?


Is dehydroepiandrosterone a hormone?
Related Articles

Is dehydroepiandrosterone a hormone?

J Endocrinol. 2005 Nov;187(2):169-96

Authors: Labrie F, Luu-The V, Bélanger A, Lin SX, Simard J, Pelletier G, Labrie C

Dehydroepiandrosterone (DHEA) is not a hormone but it is a very important prohormone secreted in large amounts by the adrenals in humans and other primates, but not in lower species. It is secreted in larger quantities than cortisol and is present in the blood at concentrations only second to cholesterol. All the enzymes required to transform DHEA into androgens and/or estrogens are expressed in a cell-specific manner in a large series of peripheral target tissues, thus permitting all androgen-sensitive and estrogen-sensitive tissues to make locally and control the intracellular levels of sex steroids according to local needs. This new field of endocrinology has been called intracrinology. In women, after menopause, all estrogens and almost all androgens are made locally in peripheral tissues from DHEA which indirectly exerts effects, among others, on bone formation, adiposity, muscle, insulin and glucose metabolism, skin, libido and well-being. In men, where the secretion of androgens by the testicles continues for life, the contribution of DHEA to androgens has been best evaluated in the prostate where about 50% of androgens are made locally from DHEA. Such knowledge has led to the development of combined androgen blockade (CAB), a treatment which adds a pure anti-androgen to medical (GnRH agonist) or surgical castration in order to block the access of the androgens made locally to the androgen receptor. In fact, CAB has been the first treatment demonstrated to prolong life in advanced prostate cancer while recent data indicate that it can permit long-term control and probably cure in at least 90% of cases of localized prostate cancer. The new field of intracrinology or local formation of sex steroids from DHEA in target tissues has permitted major advances in the treatment of the two most frequent cancers, namely breast and prostate cancer, while its potential use as a physiological HRT could well provide a physiological balance of androgens and estrogens, thus offering exciting possibilities for women's health at menopause.

PMID: 16293766 [PubMed - indexed for MEDLINE]


Posted by at 8:48 PM |

May 4, 2006

Is dehydroepiandrosterone a hormone?


Is dehydroepiandrosterone a hormone?
Related Articles

Is dehydroepiandrosterone a hormone?

J Endocrinol. 2005 Nov;187(2):169-96

Authors: Labrie F, Luu-The V, B langer A, Lin SX, Simard J, Pelletier G, Labrie C

Dehydroepiandrosterone (DHEA) is not a hormone but it is a very important prohormone secreted in large amounts by the adrenals in humans and other primates, but not in lower species. It is secreted in larger quantities than cortisol and is present in the blood at concentrations only second to cholesterol. All the enzymes required to transform DHEA into androgens and/or estrogens are expressed in a cell-specific manner in a large series of peripheral target tissues, thus permitting all androgen-sensitive and estrogen-sensitive tissues to make locally and control the intracellular levels of sex steroids according to local needs. This new field of endocrinology has been called intracrinology. In women, after menopause, all estrogens and almost all androgens are made locally in peripheral tissues from DHEA which indirectly exerts effects, among others, on bone formation, adiposity, muscle, insulin and glucose metabolism, skin, libido and well-being. In men, where the secretion of androgens by the testicles continues for life, the contribution of DHEA to androgens has been best evaluated in the prostate where about 50% of androgens are made locally from DHEA. Such knowledge has led to the development of combined androgen blockade (CAB), a treatment which adds a pure anti-androgen to medical (GnRH agonist) or surgical castration in order to block the access of the androgens made locally to the androgen receptor. In fact, CAB has been the first treatment demonstrated to prolong life in advanced prostate cancer while recent data indicate that it can permit long-term control and probably cure in at least 90% of cases of localized prostate cancer. The new field of intracrinology or local formation of sex steroids from DHEA in target tissues has permitted major advances in the treatment of the two most frequent cancers, namely breast and prostate cancer, while its potential use as a physiological HRT could well provide a physiological balance of androgens and estrogens, thus offering exciting possibilities for women's health at menopause.

PMID: 16293766 [PubMed - indexed for MEDLINE]


Posted by at 11:40 AM |

Galectin-3 regulates mitochondrial stability and antiapoptotic function in response to anticancer drug in prostate cancer.


Galectin-3 regulates mitochondrial stability and antiapoptotic function in response to anticancer drug in prostate cancer.
Related Articles

Galectin-3 regulates mitochondrial stability and antiapoptotic function in response to anticancer drug in prostate cancer.

Cancer Res. 2006 Mar 15;66(6):3114-9

Authors: Fukumori T, Oka N, Takenaka Y, Nangia-Makker P, Elsamman E, Kasai T, Shono M, Kanayama HO, Ellerhorst J, Lotan R, Raz A

Prostate cancer is one of the malignant tumors which exhibit resistance to anticancer drugs, at least in part due to enhanced antiapoptotic mechanisms. Therefore, the understanding of such mechanisms should improve the design of chemotherapy against prostate cancer. Galectin-3 (Gal-3), a multifunctional oncogenic protein involved in the regulation of tumor proliferation, angiogenesis, and apoptosis has shown antiapoptotic effects in certain cell types. Here, we show that the expression of exogenous Gal-3 in human prostate cancer LNCaP cells, which do not express Gal-3 constitutively, inhibits anticancer drug-induced apoptosis by stabilizing the mitochondria. Thus, Gal-3-negative cells showed 66.31% apoptosis after treatment with 50 micromol/L cis-diammine-dichloroplatinum for 48 hours, whereas two clones of Gal-3-expressing cells show only 2.92% and 1.42% apoptotic cells. Similarly, Gal-3-negative cells showed 43.8% apoptosis after treatment with 300 micromol/L etoposide for 48 hours, whereas only 15.38% and 14.51% of Gal-3-expressing LNCaP cells were apoptotic. The expression of Gal-3 stimulated the phosphorylation of Ser(112) of Bcl-2-associated death (Bad) protein and down-regulated Bad expression after treatment with cis-diammine-dichloroplatinum. Gal-3 also inhibited mitochondrial depolarization and damage after translocation from the nuclei to the cytoplasm, resulting in inhibition of cytochrome c release and caspase-3 activation. These findings indicate that Gal-3 inhibits anticancer drug-induced apoptosis through regulation of Bad protein and suppression of the mitochondrial apoptosis pathway. Therefore, targeting Gal-3 could improve the efficacy of anticancer drug chemotherapy in prostate cancer.

PMID: 16540661 [PubMed - indexed for MEDLINE]


Posted by at 11:40 AM |

May 2, 2006

Intra-operative prostate examination: predictive value and effect on margin status.


Intra-operative prostate examination: predictive value and effect on margin status.
Related Articles

Intra-operative prostate examination: predictive value and effect on margin status.

BJU Int. 2005 Nov;96(7):1005-8

Authors: Rapp DE, Orvieto MA, Lucioni A, Gong EM, Shalhav AL, Brendler CB

OBJECTIVE: To evaluate the ability of intra-operative prostate examination (IOPE) to predict extraprostatic extension (EPE) and its effect on margin status in the region of the neurovascular bundle (NVB) when combined with wide excision. PATIENTS AND METHODS: We retrospectively reviewed 403 patients with clinical stage T1c prostate adenocarcinoma undergoing radical retropubic prostatectomy (RRP). All patients had IOPE during RRP, and those with palpable abnormalities in the region of the NVB underwent wide excision. Pathological outcomes were analysed. RESULTS: Of 403 patients, 49 (12%) had a palpable abnormality in the region of the NVB. After wide excision, 18 (37%) of these 49 patients were found to have EPE at the site of the palpable abnormality; with wide excision of the NVB, only one of these 18 patients (6%) had a corresponding positive surgical margin (PSM). In 354 patients with a normal IOPE and who underwent bilateral NVB preservation, 30 were found to have EPE in the region of the NVB. The PSM rate in this subset was 23% (seven of 30). The positive predictive value of IOPE for detecting EPE was 37%. CONCLUSION: IOPE detects abnormalities in 12% of patients with preoperative stage T1c prostate cancer. Although the predictive value of this test is limited, IOPE may decrease PSMs in a subset of patients with EPE in the region of the NVB. The present study reaffirms the value of IOPE for assessing the risk of extraprostatic disease, and for guiding surgical management.

PMID: 16225517 [PubMed - indexed for MEDLINE]


Posted by at 4:31 PM |

(((prostate cancer treatment) AND "2005/11/13 17.56"[MHDA]:"2115/11/20 14.01"[MHDA])) NOT (( (((prostate cancer[TIAB] AND treatment[TIAB]))) AND "0001"[EDAT]:"2005/11/13 17.56"[EDAT])); +184 new citations


(((prostate cancer treatment) AND "2005/11/13 17.56"[MHDA]:"2115/11/20 14.01"[MHDA])) NOT (( (((prostate cancer[TIAB] AND treatment[TIAB]))) AND "0001"[EDAT]:"2005/11/13 17.56"[EDAT])); +184 new citations

184 new PubMed citations were retrieved for your search. Click on the search hyperlink below to display the complete search results:

(((prostate cancer treatment) AND "2005/11/13 17.56"[MHDA]:"2115/11/20 14.01"[MHDA])) NOT (( (((prostate cancer[TIAB] AND treatment[TIAB]))) AND "0001"[EDAT]:"2005/11/13 17.56"[EDAT]))

These PubMed results were generated on 2006/05/02

PubMed, a service of the National Library of Medicine, includes over 15 million citations for biomedical articles back to the 1950's. These citations are from MEDLINE and additional life science journals. PubMed includes links to many sites providing full text articles and other related resources.


Posted by at 4:31 PM |

April 18, 2006

High-affinity near-infrared fluorescent small-molecule contrast agents for in vivo imaging of prostate-specific membrane antigen.


High-affinity near-infrared fluorescent small-molecule contrast agents for in vivo imaging of prostate-specific membrane antigen.
Related Articles

High-affinity near-infrared fluorescent small-molecule contrast agents for in vivo imaging of prostate-specific membrane antigen.

Mol Imaging. 2005 Oct-Dec;4(4):448-62

Authors: Humblet V, Lapidus R, Williams LR, Tsukamoto T, Rojas C, Majer P, Hin B, Ohnishi S, De Grand AM, Zaheer A, Renze JT, Nakayama A, Slusher BS, Frangioni JV

Surgical resection remains a definitive treatment for prostate cancer. Yet, prostate cancer surgery is performed without image guidance for tumor margin, extension beyond the capsule and lymph node positivity, and without verification of other occult metastases in the surgical field. Recently, several imaging systems have been described that exploit near-infrared (NIR) fluorescent light for sensitive, real-time detection of disease pathology intraoperatively. In this study, we describe a high-affinity (9 nM), single nucleophile-containing, small molecule specific for the active site of the enzyme PSMA. We demonstrate production of a tetra-sulfonated heptamethine indocyanine NIR fluorescent derivative of this molecule using a high-yield LC/MS purification strategy. Interestingly, NIR fluorophore conjugation improves affinity over 20-fold, and we provide mechanistic insight into this observation. We describe the preparative production of enzymatically active PSMA using a baculovirus expression system and an adenovirus that co-expresses PSMA and GFP. We demonstrate sensitive and specific in vitro imaging of endogenous and ectopically expressed PSMA in human cells and in vivo imaging of xenograft tumors. We also discuss chemical strategies for improving performance even further. Taken together, this study describes nearly complete preclinical development of an optically based small-molecule contrast agent for image-guided surgery.

PMID: 16285907 [PubMed - indexed for MEDLINE]


Posted by at 5:56 PM |

Hand-assisted laparoscopic cystoprostatectomy and urinary diversion.


Hand-assisted laparoscopic cystoprostatectomy and urinary diversion.
Related Articles

Hand-assisted laparoscopic cystoprostatectomy and urinary diversion.

J Urol. 2005 Nov;174(5):1859-60

Authors: Smith JA

PMID: 16217321 [PubMed - indexed for MEDLINE]


Posted by at 5:37 PM |

Profiling alternatively spliced mRNA isoforms for prostate cancer classification.


Profiling alternatively spliced mRNA isoforms for prostate cancer classification.
Related Articles

Profiling alternatively spliced mRNA isoforms for prostate cancer classification.

BMC Bioinformatics. 2006 Apr 11;7(1):202

Authors: Zhang C, Li HR, Fan JB, Wang-Rodriguez J, Downs T, Fu XD, Zhang MQ

ABSTRACT: BACKGROUND: Prostate cancer is one of the leading causes of cancer illness and death among men in the United States and world wide. There is an urgent need to discover good biomarkers for early clinical diagnosis and treatment. Previously, we developed an exon-junction microarray-based assay and profiled 1532 mRNA splice isoforms from 364 potential prostate cancer related genes in 38 prostate tissues. Here, we investigate the advantage of using splice isoforms, which couple transcriptional and splicing regulation, for cancer classification. RESULTS: As many as 464 splice isoforms from more than 200 genes are differentially regulated in tumors at a false discovery rate (FDR) of 0.05. Remarkably, about 30% of genes have isoforms that are called significant but do not exhibit differential expression at the overall mRNA level. A support vector machine (SVM) classifier trained on 128 signature isoforms can correctly predict 92% of the cases, which outperforms the classifier using overall mRNA abundance by about 5%. It is also observed that the classification performance can be improved using multivariate variable selection methods, which take correlation among variables into account. CONCLUSIONS: These results demonstrate that profiling of splice isoforms is able to provide unique and important information which cannot be detected by conventional microarrays.

PMID: 16608523 [PubMed - as supplied by publisher]


Posted by at 5:37 PM |

April 12, 2006

Randomized, placebo-controlled trial showing that finasteride reduces prostatic vascularity rapidly within 2 weeks.


Randomized, placebo-controlled trial showing that finasteride reduces prostatic vascularity rapidly within 2 weeks.
Related Articles

Randomized, placebo-controlled trial showing that finasteride reduces prostatic vascularity rapidly within 2 weeks.

BJU Int. 2005 Dec;96(9):1319-22

Authors: Donohue JF, Hayne D, Karnik U, Thomas DR, Foster MC

OBJECTIVE: To measure expression of vascular endothelial growth factor (VEGF) and microvessel density (MVD) in the prostates of men after transurethral resection of the prostate (TURP) following 2 weeks of treatment with finasteride. PATIENTS AND METHODS: Sixty-four men scheduled to undergo TURP were randomized to receive 5 mg of finasteride or placebo daily for 2 weeks before surgery. Sections of prostatic urothelium were stained for VEGF expression and for CD31 to assess MVD. Ten consecutive, non-overlapping high-power fields were analysed in a blinded fashion. RESULTS: In all, 31 men received finasteride and 33 placebo; the groups were similar in patient age, resected prostate weight, preoperative catheterization, prostate-specific antigen level, aspirin use, spinal anaesthesia and postoperative diagnosis of prostate cancer. The mean (95% confidence interval) MVD was significantly lower in the finasteride group (60, 55-65) than in the placebo group (71, 64-78; P < 0.01). Similarly, the mean expression of VEGF was significantly lower in the finasteride group (47, 43-52 vs 61, 54-67; P < 0.001) CONCLUSION: Finasteride inhibits angiogenic growth factors leading to reduced vascularity, and this is the basis of its action in reducing haematuria of prostatic origin. The present study shows that finasteride influences the prostatic microvasculature after only 2 weeks exposure.

PMID: 16287453 [PubMed - indexed for MEDLINE]


Posted by at 11:17 PM |

(((prostate cancer treatment) AND "2005/11/13 17.56"[MHDA]:"2115/11/20 14.01"[MHDA])) NOT (( (((prostate cancer[TIAB] AND treatment[TIAB]))) AND "0001"[EDAT]:"2005/11/13 17.56"[EDAT])); +73 new citations


(((prostate cancer treatment) AND "2005/11/13 17.56"[MHDA]:"2115/11/20 14.01"[MHDA])) NOT (( (((prostate cancer[TIAB] AND treatment[TIAB]))) AND "0001"[EDAT]:"2005/11/13 17.56"[EDAT])); +73 new citations

73 new PubMed citations were retrieved for your search. Click on the search hyperlink below to display the complete search results:

(((prostate cancer treatment) AND "2005/11/13 17.56"[MHDA]:"2115/11/20 14.01"[MHDA])) NOT (( (((prostate cancer[TIAB] AND treatment[TIAB]))) AND "0001"[EDAT]:"2005/11/13 17.56"[EDAT]))

These PubMed results were generated on 2006/04/13

PubMed, a service of the National Library of Medicine, includes over 15 million citations for biomedical articles back to the 1950's. These citations are from MEDLINE and additional life science journals. PubMed includes links to many sites providing full text articles and other related resources.


Posted by at 11:17 PM |

April 5, 2006

Pretreatment predictors of posttreatment PSA doubling times for patients undergoing three-dimensional conformal radiotherapy for clinically localized prostate cancer.


Pretreatment predictors of posttreatment PSA doubling times for patients undergoing three-dimensional conformal radiotherapy for clinically localized prostate cancer.
Related Articles

Pretreatment predictors of posttreatment PSA doubling times for patients undergoing three-dimensional conformal radiotherapy for clinically localized prostate cancer.

Urology. 2005 Nov;66(5):1020-3

Authors: Beard C, Chen MH, Cote K, Loffredo M, Renshaw A, Hurwitz M, D'Amico AV

OBJECTIVES: To determine whether pretreatment risk groups also predict for posttreatment prostate-specific antigen (PSA) doubling times (PSADTs). Pretreatment risk groups predict for posttreatment biochemical failure (BF) after conformal radiotherapy in patients with prostate cancer and posttreatment PSADTs can predict for prostate cancer-related deaths. METHODS: The study cohort consisted of 416 patients with clinically localized prostate cancer treated with conformal radiotherapy between 1989 and 2001. The patients were divided into low, intermediate, and high-risk groups. BF was defined using the American Society for Therapeutic Radiology and Oncology consensus definition. Patients with BF were grouped according to their PSADT (3 months or less, longer than 3 months to less than 6 months, 6 months to less than 12 months, and 12 months or longer). A Mantle-Haenszel chi-square metric tested for an association between the pretreatment risk group and the PSADT. Logistic regression multivariate analysis was performed to evaluate whether the pretreatment risk group predicted the PSADT. RESULTS: Of the 416 patients, 96 (23%), 194 (47%), and 126 (30%) were categorized as low, intermediate, and high risk, respectively. A total of 92 patients (22%) experienced BF. Of these 92 patients, the PSADT was 3 months or less in 6 (7%), longer than 3 months to less than 6 months in 13 (14%), 6 months to less than 12 months in 35 (36%), and 12 months or longer in 38 (41%). The pretreatment risk group correlated significantly with the PSADT (P = 0.026). Logistic regression analysis revealed that intermediate and high-risk disease was significantly associated with shorter PSADTs (P = 0.039). CONCLUSIONS: A significant association between the pretreatment risk group and posttreatment PSADT was demonstrated. Use of this selection criterion at diagnosis for more aggressive treatment appears warranted.

PMID: 16286116 [PubMed - indexed for MEDLINE]


Posted by at 10:32 AM |

(((prostate cancer treatment) AND "2005/11/13 17.56"[MHDA]:"2115/11/20 14.01"[MHDA])) NOT (( (((prostate cancer[TIAB] AND treatment[TIAB]))) AND "0001"[EDAT]:"2005/11/13 17.56"[EDAT])); +165 new citations


(((prostate cancer treatment) AND "2005/11/13 17.56"[MHDA]:"2115/11/20 14.01"[MHDA])) NOT (( (((prostate cancer[TIAB] AND treatment[TIAB]))) AND "0001"[EDAT]:"2005/11/13 17.56"[EDAT])); +165 new citations

165 new PubMed citations were retrieved for your search. Click on the search hyperlink below to display the complete search results:

(((prostate cancer treatment) AND "2005/11/13 17.56"[MHDA]:"2115/11/20 14.01"[MHDA])) NOT (( (((prostate cancer[TIAB] AND treatment[TIAB]))) AND "0001"[EDAT]:"2005/11/13 17.56"[EDAT]))

These PubMed results were generated on 2006/04/05

PubMed, a service of the National Library of Medicine, includes over 15 million citations for biomedical articles back to the 1950's. These citations are from MEDLINE and additional life science journals. PubMed includes links to many sites providing full text articles and other related resources.


Posted by at 10:31 AM |

March 21, 2006

Factors contributing to the racial differences in prostate cancer mortality.


Factors contributing to the racial differences in prostate cancer mortality.
Related Articles Factors contributing to the racial differences in prostate cancer mortality. BJU Int. 2005 Dec;96(9):1247-52 Authors: Tewari A, Horninger W, Pelzer AE, Demers R, Crawford ED, Gamito EJ, Divine G, Johnson CC, Bartsch G, Menon M OBJECTIVE: To analyse, in a retrospective cohort study, differences in rates of surgical treatment for prostate cancer between African-Americans and White Americans, and to evaluate the extent to which these differences are associated with disparities in survival rates between these groups. PATIENTS AND METHODS: Clinical, pathological, and demographic data from 4279 men diagnosed with clinically localized prostate cancer between 1980 and 1997 were used. The variables assessed included age, disease stage, tumour grade, comorbidities, treatment method, and socio-economic status (SES). Kaplan-Meier survival curves were generated and compared using log-rank tests. The Cox proportional hazards method was used for analyses involving adjustments for potential confounding factors. RESULTS: The surgical treatment rate was 17% for African-American and 28% for White patients (P < 0.001). In those patients treated conservatively or by radiation therapy, both crude and cancer-specific survival rates were lower for African-Americans than for Whites (P < 0.001). However, for patients undergoing surgery, differences in survival between African-Americans and Whites were not statistically significant. According to our models, SES explained 50% and surgical treatment rates approximately 34% of the differences in survival between African-Americans and Whites. CONCLUSIONS: This analysis suggests that the lower prostate cancer survival rates for the African-Americans in the present population can be largely explained by differences in SES and lower surgical treatment rates. Efforts to increase awareness of treatment options among African-American patients may be a way of improving survival in this group. PMID: 16287439 [PubMed - indexed for MEDLINE]

Posted by at 11:42 PM |

A dosimetric comparison of 169Yb versus 192Ir for HDR prostate brachytherapy.


A dosimetric comparison of 169Yb versus 192Ir for HDR prostate brachytherapy.
Related Articles A dosimetric comparison of 169Yb versus 192Ir for HDR prostate brachytherapy. Med Phys. 2005 Dec;32(12):3832-42 Authors: Lymperopoulou G, Papagiannis P, Sakelliou L, Milickovic N, Giannouli S, Baltas D For the purpose of evaluating the use of 169Yb for prostate High Dose Rate brachytherapy (HDR), a hypothetical 169Yb source is assumed with the exact same design of the new microSelectron source replacing the 192Ir active core by pure 169Yb metal. Monte Carlo simulation is employed for the full dosimetric characterization of both sources and results are compared following the AAPM TG-43 dosimetric formalism. Monte Carlo calculated dosimetry results are incorporated in a commercially available treatment planning system (SWIFT), which features an inverse treatment planning option based on a multiobjective dose optimization engine. The quality of prostate HDR brachytherapy using the real 192Ir and hypothetical 169Yb source is compared in a comprehensive analysis of different prostate implants in terms of the multiobjective dose optimization solutions as well as treatment quality indices such as Dose Volume Histograms (DVH) and the Conformal Index (COIN). Given that scattering overcompensates for absorption in intermediate photon energies and distances in the range of interest to prostate HDR brachytherapy, 169Yb proves at least equivalent to 192Ir irrespective of prostate volume. This has to be evaluated in view of the shielding requirements for the 169Yb energies that are minimal relative to that for 192Ir. PMID: 16475783 [PubMed - indexed for MEDLINE]

Posted by at 11:42 PM |

March 16, 2006

Promise for prostatitis?


Promise for prostatitis?
Related Articles Promise for prostatitis? BJU Int. 2005 Nov;96(7):1137-8 Authors: Wyllie MG PMID: 16225543 [PubMed - indexed for MEDLINE]

Posted by at 10:08 AM |

Genitourinary small cell carcinoma: a retrospective review of treatment and survival patterns at The Ottawa Hospital Regional Cancer Center.


Genitourinary small cell carcinoma: a retrospective review of treatment and survival patterns at The Ottawa Hospital Regional Cancer Center.
Genitourinary small cell carcinoma: a retrospective review of treatment and survival patterns at The Ottawa Hospital Regional Cancer Center. BJU Int. 2006 Apr;97(4):711-5 Authors: Asmis TR, Reaume MN, Dahrouge S, Malone S OBJECTIVE To review patients with genitourinary (GU) small cell carcinoma (SCC) treated at a regional cancer centre, as due to its rarity and aggressive nature, GU SCC remains a therapeutic challenge. PATIENTS AND METHODS The charts of patients managed at a regional cancer centre between 1991 and 2002 for any GU diagnosis were manually reviewed to identify GU SCC. Demographic, staging, treatment and outcome data were extracted. The Veterans Administration small cell lung cancer staging classification of 'limited' or 'extensive' disease was adapted for SCC of the prostate and bladder (with 'limited' defined as disease localized to the true and false pelvis, and 'extensive' as disease beyond the pelvis). RESULTS In all, 555, 858 and 5066 new cases of primary renal, bladder and prostate cancer, respectively, were identified. Of these patients, 22 had GU SCC (12 bladder and 10 prostate; there were no cases of SCC of the kidney). Eight of 12 patients with bladder SCC had limited disease; five of 12 are alive (all with limited disease at diagnosis), and the median survival was 19.8 months. Surviving patients received similar therapy, with transurethral resection of the bladder tumour, platinum-based chemotherapy, etoposide (4-6 cycles), and radical radiotherapy (56-60 Gy). Two of 10 patients with SCC of the prostate had limited-stage disease, but all 10 died, the median survival being 9.5 months. Survival by stage for both types combined was 59 months for limited disease and 8 months for extensive disease. CONCLUSIONS These results indicate that GU SCC is an aggressive cancer; limited-stage SCC of the bladder or prostate, when treated with platinum/etoposide chemotherapy and radical radiotherapy, has a more favourable outcome than that of extensive GU SCC. PMID: 16536759 [PubMed - in process]

Posted by at 10:08 AM |

March 15, 2006

Non-genomic effects of the androgen receptor and Vitamin D agonist are involved in suppressing invasive phenotype of prostate cancer cells.


Non-genomic effects of the androgen receptor and Vitamin D agonist are involved in suppressing invasive phenotype of prostate cancer cells.
Related Articles Non-genomic effects of the androgen receptor and Vitamin D agonist are involved in suppressing invasive phenotype of prostate cancer cells. Steroids. 2005 Nov 8; Authors: Bonaccorsi L, Marchiani S, Ferruzzi P, Muratori M, Crescioli C, Forti G, Maggi M, Baldi E Suppression of invasive phenotype is essential in developing new therapeutic tools to treat prostate cancer (PC). Evidence indicates that androgen-dependent (AD) prostate cancer cells are characterized by a lower malignant phenotype. We have demonstrated that transfection with an androgen receptor (AR) expression vector of the androgen-independent (AI) prostate cancer cell line PC3 decreases invasion of these cells through modulation of alpha6beta4 integrin expression, indicating a genotropic effect of androgens in inhibiting invasion ability of AD PC cells. Later on, we have shown that also a non-genotropic mechanism is involved in such an effect. By using immunoconfocal fluorescent microscopy, we demonstrated that AR in PC3-AR cells co-localizes with the EGFR receptors (EGFR) in PC3-AR cells. Co-immunoprecipitation studies both in PC3-AR cells and in the AD cell line LNCaP that physiologically express both receptors, confirm the occurrence of an interaction between of the two proteins. In PC3-AR cells, we demonstrated a disruption of EGFR signalling properties (reduced EGF-induced EGFR autotransphosphorylation, reduced EGF-stimulated PI3K activity as well as EGFR-PI3K interaction) contributing to the lower invasive phenotype of these cells. In another study, we investigated the effects of a new Vitamin D analogue, BXL628, on invasion in response to KGF in the androgen-independent PC cell line DU145. We found that the compound was able to reduce proliferation and invasion of the cells in response to the growth factor. In addition, we found that KGF-induced autotransphosphorylation of KGF receptor (KGFR) and PI3K activation were suppressed after short-term (5min) pre-treatment with the analogue before addition of KGF. Collectively, these studies demonstrate that a non-genotropic effect due to a direct interaction of the androgen receptor with EGFR and to a rapid effect of a Vitamin D agonist on KGFR may disrupt signalling of GF leading to decreased tumorigenicity and a less malignant phenotype of PC cells in vitro. PMID: 16289173 [PubMed - as supplied by publisher]

Posted by at 12:37 PM |

Quercetin-induced growth inhibition and cell death in prostatic carcinoma cells (PC-3) are associated with increase in p21 and hypophosphorylated retinoblastoma proteins expression.


Quercetin-induced growth inhibition and cell death in prostatic carcinoma cells (PC-3) are associated with increase in p21 and hypophosphorylated retinoblastoma proteins expression.
Related Articles Quercetin-induced growth inhibition and cell death in prostatic carcinoma cells (PC-3) are associated with increase in p21 and hypophosphorylated retinoblastoma proteins expression. J Cancer Res Clin Oncol. 2005 Nov;131(11):765-71 Authors: Vijayababu MR, Kanagaraj P, Arunkumar A, Ilangovan R, Aruldhas MM, Arunakaran J Prostate cancer is the major health problem and the leading cause of male cancer death. Quercetin is a novel antitumor and antioxidant, whose molecular mechanism involved in cell cycle arrest in androgen independent prostate cancer cells remains unclear. In this study, we investigated the effects of quercetin on proliferation and cell cycle arrest by modulation of Cdc2/Cdk-1 protein in prostate cancer cells (PC-3). PC- 3 cells are human androgen independent cancer cells and were cultured with quercetin at concentrations of 50 and 100 microM for 24 h. Cell proliferation, apoptosis and cell cycle distribution were analyzed. Expression of Cdc2/Cdk-1, cyclin B1, cyclin A, p21/Cip1, pRb, pRb2/p130, Bcl-2, Bcl-X(L), Bax and caspase-3 proteins were studied with western blot analysis. Addition of quercetin led to substantial decrease in the expression of Cdc2/Cdk-1, cyclin B1 and phosphorylated pRb and increase in p21. Flowcytometric analysis showed that quercetin blocks G2-M transition, with significant induction of apoptosis. Apoptosis markers like Bcl-2 and Bcl-X(L) were significantly decreased and Bax and caspase-3 were increased. From this study, it was concluded that quercetin inhibits prostate cancer cell proliferation by altering the expression of cell cycle regulators and apoptotic proteins. PMID: 16049707 [PubMed - indexed for MEDLINE]

Posted by at 12:37 PM |

March 12, 2006

Factors contributing to the racial differences in prostate cancer mortality.


Factors contributing to the racial differences in prostate cancer mortality.
Related Articles Factors contributing to the racial differences in prostate cancer mortality. BJU Int. 2005 Dec;96(9):1247-52 Authors: Tewari A, Horninger W, Pelzer AE, Demers R, Crawford ED, Gamito EJ, Divine G, Johnson CC, Bartsch G, Menon M OBJECTIVE: To analyse, in a retrospective cohort study, differences in rates of surgical treatment for prostate cancer between African-Americans and White Americans, and to evaluate the extent to which these differences are associated with disparities in survival rates between these groups. PATIENTS AND METHODS: Clinical, pathological, and demographic data from 4279 men diagnosed with clinically localized prostate cancer between 1980 and 1997 were used. The variables assessed included age, disease stage, tumour grade, comorbidities, treatment method, and socio-economic status (SES). Kaplan-Meier survival curves were generated and compared using log-rank tests. The Cox proportional hazards method was used for analyses involving adjustments for potential confounding factors. RESULTS: The surgical treatment rate was 17% for African-American and 28% for White patients (P < 0.001). In those patients treated conservatively or by radiation therapy, both crude and cancer-specific survival rates were lower for African-Americans than for Whites (P < 0.001). However, for patients undergoing surgery, differences in survival between African-Americans and Whites were not statistically significant. According to our models, SES explained 50% and surgical treatment rates approximately 34% of the differences in survival between African-Americans and Whites. CONCLUSIONS: This analysis suggests that the lower prostate cancer survival rates for the African-Americans in the present population can be largely explained by differences in SES and lower surgical treatment rates. Efforts to increase awareness of treatment options among African-American patients may be a way of improving survival in this group. PMID: 16287439 [PubMed - indexed for MEDLINE]

Posted by at 7:44 PM |

(((prostate cancer treatment) AND "2005/11/13 17.56"[MHDA]:"2115/11/20 14.01"[MHDA])) NOT (( (((prostate cancer[TIAB] AND treatment[TIAB]))) AND "0001"[EDAT]:"2005/11/13 17.56"[EDAT])); +262 new citations


(((prostate cancer treatment) AND "2005/11/13 17.56"[MHDA]:"2115/11/20 14.01"[MHDA])) NOT (( (((prostate cancer[TIAB] AND treatment[TIAB]))) AND "0001"[EDAT]:"2005/11/13 17.56"[EDAT])); +262 new citations
262 new PubMed citations were retrieved for your search. Click on the search hyperlink below to display the complete search results: (((prostate cancer treatment) AND "2005/11/13 17.56"[MHDA]:"2115/11/20 14.01"[MHDA])) NOT (( (((prostate cancer[TIAB] AND treatment[TIAB]))) AND "0001"[EDAT]:"2005/11/13 17.56"[EDAT])) These PubMed results were generated on 2006/03/12PubMed, a service of the National Library of Medicine, includes over 15 million citations for biomedical articles back to the 1950's. These citations are from MEDLINE and additional life science journals. PubMed includes links to many sites providing full text articles and other related resources.

Posted by at 7:44 PM |

February 27, 2006

Can docetaxel plus estramustine prolong survival of men with metastatic hormone-refractory prostate cancer?


Can docetaxel plus estramustine prolong survival of men with metastatic hormone-refractory prostate cancer?
Related Articles Can docetaxel plus estramustine prolong survival of men with metastatic hormone-refractory prostate cancer? Nat Clin Pract Oncol. 2005 Feb;2(2):70-1 Authors: Sleijfer S, Stoter G PMID: 16264874 [PubMed - indexed for MEDLINE]

Posted by at 8:29 PM |

February 20, 2006

Development and evaluation of a prostate sexual rehabilitation clinic: a pilot project.


Development and evaluation of a prostate sexual rehabilitation clinic: a pilot project.
Related Articles Development and evaluation of a prostate sexual rehabilitation clinic: a pilot project. BJU Int. 2005 Dec;96(9):1360-4 Authors: Davison BJ, Elliott S, Ekland M, Griffin S, Wiens K OBJECTIVE: To evaluate a sexual rehabilitation service for men with prostate cancer and to use these results to inform the development of future care. PATIENTS AND METHODS: The study participants included 155 men with prostate cancer referred to a sexual rehabilitation clinic by their urologists or radiation oncologists, of whom the partners of 58 were in attendance. Questionnaires to measure sexual function and positive feelings towards the partner were completed before the clinic visit; and for satisfaction with the clinic service immediately after the appointment; and for sexual function, positive feelings towards the partner, and satisfaction with treatments at 4 months afterward. RESULTS: Ninety patients completed the 4-month evaluation, of whom 35 were couples. Enhancement of erection and understanding sexual changes related to treatment were the two main concerns of patients. Phosphodiesterase-5 inhibitors and intracavernosal injections were the treatments of choice. Compared with partners, patients had significantly greater positive feelings towards their partners at both measurement times and were more satisfied with their prescribed treatment. The total scores on sexual function were significantly higher at 4 months. CONCLUSIONS: These results support the need to include partners as a necessary part of these men's sexual rehabilitation. A structured follow-up is necessary to monitor the success of treatment and to document the quality of erection. PMID: 16287458 [PubMed - indexed for MEDLINE]

Posted by at 1:37 PM |

Frequent high-level expression of the immunotherapeutic target Ep-CAM in colon, stomach, prostate and lung cancers.


Frequent high-level expression of the immunotherapeutic target Ep-CAM in colon, stomach, prostate and lung cancers.
Related Articles Frequent high-level expression of the immunotherapeutic target Ep-CAM in colon, stomach, prostate and lung cancers. Br J Cancer. 2006 Jan 16;94(1):128-35 Authors: Went P, Vasei M, Bubendorf L, Terracciano L, Tornillo L, Riede U, Kononen J, Simon R, Sauter G, Baeuerle PA Epithelial cell adhesion molecule (Ep-CAM; CD326) is used as a target by many immunotherapeutic approaches, but little data are available about Ep-CAM expression in major human malignancies with respect to level, frequency, tumour stage, grade, histologic tumour type and impact on survival. We analysed by immunohistochemical staining tissue microarrays with 4046 primary human carcinoma samples from colon, stomach, prostate and lung cancers for both frequency and intensity of Ep-CAM expression under highly standardised conditions. A total of 3360 samples were analysable. High-level Ep-CAM expression was observed in 97.7% (n=1186) of colon, 90.7% of gastric (n=473), and 87.2% of prostate cancers (n=414), and in 63.9% of lung cancers (n=1287). No detectable Ep-CAM staining was found with only 0.4% of colon, 2.5% of gastric, 1.9% of prostate cancers, and 13.5% of lung cancers. The only significant correlation of Ep-CAM expression with tumour grading was observed in colon cancer where high-level Ep-CAM expression on grade 3 tumours was down to 92.1% (P<0.0001). Adenosquamous and squamous carcinomas of the lung had a lower percentage of high-level Ep-CAM expression compared to adenocarcinomas with 35.4 and 53.6%, respectively, and with 45.5 and 17.3% of tumours being Ep-CAM negative. With the exception of moderately differentiated colon carcinoma, where patients not expressing Ep-CAM on their tumours showed an inferior survival (P=0.0014), correlation of Ep-CAM expression with survival did not reach statistical significance for any of the other cancer indications and subgroups. In conclusion, the data strongly support the notion that Ep-CAM is a prime target for immunotherapies in major human malignancies. This is because the most common human cancers show (i) a low frequency of Ep-CAM-negative tumours, (ii) a high frequency of Ep-CAM expression on cells of a given tumour, and (iii) for most cancers, an insignificant influence of tumour staging, grading and histology on Ep-CAM expression. PMID: 16404366 [PubMed - indexed for MEDLINE]

Posted by at 1:37 PM |

February 15, 2006

Intra-operative prostate examination: predictive value and effect on margin status.


Intra-operative prostate examination: predictive value and effect on margin status.
Related Articles Intra-operative prostate examination: predictive value and effect on margin status. BJU Int. 2005 Nov;96(7):1005-8 Authors: Rapp DE, Orvieto MA, Lucioni A, Gong EM, Shalhav AL, Brendler CB OBJECTIVE: To evaluate the ability of intra-operative prostate examination (IOPE) to predict extraprostatic extension (EPE) and its effect on margin status in the region of the neurovascular bundle (NVB) when combined with wide excision. PATIENTS AND METHODS: We retrospectively reviewed 403 patients with clinical stage T1c prostate adenocarcinoma undergoing radical retropubic prostatectomy (RRP). All patients had IOPE during RRP, and those with palpable abnormalities in the region of the NVB underwent wide excision. Pathological outcomes were analysed. RESULTS: Of 403 patients, 49 (12%) had a palpable abnormality in the region of the NVB. After wide excision, 18 (37%) of these 49 patients were found to have EPE at the site of the palpable abnormality; with wide excision of the NVB, only one of these 18 patients (6%) had a corresponding positive surgical margin (PSM). In 354 patients with a normal IOPE and who underwent bilateral NVB preservation, 30 were found to have EPE in the region of the NVB. The PSM rate in this subset was 23% (seven of 30). The positive predictive value of IOPE for detecting EPE was 37%. CONCLUSION: IOPE detects abnormalities in 12% of patients with preoperative stage T1c prostate cancer. Although the predictive value of this test is limited, IOPE may decrease PSMs in a subset of patients with EPE in the region of the NVB. The present study reaffirms the value of IOPE for assessing the risk of extraprostatic disease, and for guiding surgical management. PMID: 16225517 [PubMed - indexed for MEDLINE]

Posted by at 1:42 PM |

Advanced refractory prostate cancer: new treatment trial.


Advanced refractory prostate cancer: new treatment trial.
Related Articles Advanced refractory prostate cancer: new treatment trial. Nat Clin Pract Urol. 2004 Dec;1(2):64-5 Authors: PMID: 16474510 [PubMed - in process]

Posted by at 1:41 PM |

February 14, 2006

Clinical staging of prostate cancer: a computer-simulated study of transperineal prostate biopsy.


Clinical staging of prostate cancer: a computer-simulated study of transperineal prostate biopsy.
Related Articles Clinical staging of prostate cancer: a computer-simulated study of transperineal prostate biopsy. BJU Int. 2005 Nov;96(7):999-1004 Authors: Crawford ED, Wilson SS, Torkko KC, Hirano D, Stewart JS, Brammell C, Wilson RS, Kawata N, Sullivan H, Lucia MS, Werahera PN OBJECTIVE: To identify the precise location of prostate cancer within the gland and thus possibly permit more aggressive therapy of the lesion, while potentially sparing the noncancerous gland from ablative therapy. MATERIALS AND METHODS: Three-dimensional "solid" computer models were reconstructed for 86 autopsy specimens and 20 stage T1c radical prostatectomy specimens. Transperineal biopsies were simulated for grid sizes of 5-mm (method A) and 10-mm (method B) with an 18 G, 23-mm long biopsy needle. One or two biopsies per grid point were obtained for a total of 12-108 biopsies, depending on the size of the prostate. Clinically threatening cancers were defined as having volumes of > or = 0.5 mL or Gleason sum > or = 7. RESULTS: Method A detected significantly more carcinomas than method B in both the autopsy and prostatectomy specimens (autopsy, 72 vs 51; prostatectomy, 50 vs 32, both P < 0.001). Method A also detected more clinically threatening cancers found at autopsy (38/40 vs 31/40, P = 0.008). Among autopsy patients with negative sextant biopsies whose disease was localized to one side, method A detected 72% and method B detected 29-43% (P < 0.001). CONCLUSIONS: The results of this computer simulation show that 5- and 10-mm grid biopsies detect three-quarters and a third, respectively, at autopsy, of patients with the disease localized to one side of the prostate, which may be useful when planning highly selective ablative treatments in the future. PMID: 16225516 [PubMed - indexed for MEDLINE]

Posted by at 9:09 PM |

An educational workshop on the early detection of prostate cancer--a before-after evaluation.


An educational workshop on the early detection of prostate cancer--a before-after evaluation.
Related Articles An educational workshop on the early detection of prostate cancer--a before-after evaluation. Aust Fam Physician. 2005 Oct;34(10):889-91 Authors: Steginga SK, Pinnock C, Baade PD, Jackson C, Green A, Preston J, Heathcote P, McAvoy B PMID: 16217583 [PubMed - indexed for MEDLINE]

Posted by at 9:08 PM |

Intermittent androgen ablation in patients with biochemical failure after pelvic radiotherapy for localized prostate cancer.


Intermittent androgen ablation in patients with biochemical failure after pelvic radiotherapy for localized prostate cancer.
Related Articles Intermittent androgen ablation in patients with biochemical failure after pelvic radiotherapy for localized prostate cancer. Int J Radiat Oncol Biol Phys. 2006 Mar 1;64(3):842-8 Authors: Cury FL, Souhami L, Rajan R, Tanguay S, Gagnon B, Duclos M, Shenouda G, Faria SL, David M, Freeman CR Purpose: To assess the efficacy of intermittent androgen ablation (IAA) in patients with biochemical failure after radiotherapy for prostate cancer. Methods and Materials: Thirty-nine patients received a luteinizing hormone-releasing hormone analog every 2 months for a total of 4 doses. IAA was then discontinued if serum prostate-specific antigen (PSA) fell to a normal level with a castrate level of testosterone. Therapy was restarted when the serum PSA level reached >/=10 ng/mL and was discontinued if hormone resistance or unacceptable toxicity occurred. Results: Median PSA was 9.1 ng/mL at the time of first IAA. The median time between the first and the second cycles was 20.1 months, decreasing to 15.5 months between the third and fourth cycles. Two patients discontinued the treatment because of severe hot flushes. Four patients developed hormone resistance. With a median follow-up of 56.4 months, 5-year survival is 92.3%. Three patients died of unrelated causes. The incidence of distant metastasis is 6.8%. Conclusions: The use of IAA seems to be a safe and effective treatment for patients with biochemical failure post radiotherapy and no evidence of metastatic disease. The use of IAA limits hormone-related side effects and health care costs without an apparent increase in the risk for the development of metastatic disease. PMID: 16289909 [PubMed - in process]

Posted by at 2:47 PM |

Management of clinically localized prostate cancer by radical prostatectomy followed by watchful waiting.


Management of clinically localized prostate cancer by radical prostatectomy followed by watchful waiting.
Related Articles Management of clinically localized prostate cancer by radical prostatectomy followed by watchful waiting. Nat Clin Pract Urol. 2005 Jun;2(6):298-303 Authors: Kirby R Background A 65-year-old married man requested a PSA screening test and was found to have an elevated PSA level of 5.26 ng/ml.Investigations Digital rectal examination, sextant biopsy, bone scan, and MRI to confirm diagnosis and stage the disease. Subsequent histopathologic examination of the excised prostate.Diagnosis Preoperative stage cT2b prostate cancer (Gleason score 7 [3 + 4]). Postoperative stage pT3b, N0, M0 prostate cancer (Gleason score 9 [4 + 5]), with extensive cancer within the left side of the prostate gland, involving several of the surgical margins and extending to the proximal portion of the left seminal vesicle.Management Open radical retropubic prostatectomy, then watchful waiting with further treatment deferred until disease progression. Postoperative erectile dysfunction treated with sildenafil plus prostaglandin E(1) combination therapy. PMID: 16474812 [PubMed - in process]

Posted by at 2:47 PM |

February 13, 2006

Multidisciplinary treatment of synchronous primary rectal and prostate cancers.


Multidisciplinary treatment of synchronous primary rectal and prostate cancers.
Related Articles Multidisciplinary treatment of synchronous primary rectal and prostate cancers. Nat Clin Pract Oncol. 2005 May;2(5):271-4; quiz 1 p following 274 Authors: Colonias A, Farinash L, Miller L, Jones S, Medich DS, Greenberg L, Miller R, Parda DS BACKGROUND: A 58-year-old Caucasian man with a history of irritable bowel syndrome and occasional rectal bleeding presented with a 4-week history of progressive, bright red blood per rectum. A digital rectal examination revealed a 3 cm distal, midrectal mass. Laboratory tests showed an elevated serum prostate-specific antigen of 32 ng/ml but other physical and medical examinations were unremarkable. INVESTIGATIONS: Digital rectal examination, colonoscopy, rectal mass biopsy, endorectal ultrasound, transrectal ultrasound-guided prostate biopsy, CT scan and MRI. DIAGNOSIS: Clinical stage III (T3N1M0), moderately differentiated adenocarcinoma of the rectum and clinical stage II (T1cN0M0) adenocarcinoma of the prostate. MANAGEMENT: Intensity-modulated radiation therapy, chemoradiation, chemotherapy, hormone therapy and surgery. PMID: 16264963 [PubMed - indexed for MEDLINE]

Posted by at 8:09 PM |

The significance of tumor heterogeneity for prediction of DNA ploidy of prostate cancer.


The significance of tumor heterogeneity for prediction of DNA ploidy of prostate cancer.
Related Articles The significance of tumor heterogeneity for prediction of DNA ploidy of prostate cancer. Scand J Urol Nephrol. 2005;39(5):387-92 Authors: H ggarth L, Auer G, Busch C, Norberg M, H ggman M, Egevad L OBJECTIVE: In a previous study, we mapped the ploidy heterogeneity of prostate cancer using flow cytometry in 676 tumor samples from 50 radical prostatectomy specimens. Ploidy heterogeneity was common (42% of tumors) and was found in all non-diploid tumors. The volume of non-diploid tumor was estimated and found to predict extra-prostatic extension and seminal vesicle invasion. The aim of this study was to evaluate the impact of tumor heterogeneity on preoperative ploidy assessment. MATERIAL AND METHODS: In 50 men at least six core biopsies were taken before prostatectomy. Sections from biopsies with cancer were Feulgen-stained for image cytometry. After exclusion of biopsies with insufficient material, 123 histograms from 48 men (mean 2.6; range 1-7) remained for analysis. RESULTS: In 32 men, biopsies were diploid. In 16 men, at least one biopsy was non-diploid (14 tetraploid, two aneuploid) and 10 of them also had diploid biopsies. In 34 men (71%), the prostatectomy specimens were correctly predicted as being either diploid (48%) or non-diploid (23%). The sensitivity and specificity of biopsies for predicting non-diploid cancer were 55% and 82%, respectively, and the positive and negative predictive values were 69% and 72%, respectively. The ploidy status of tumors with and without ploidy heterogeneity was correctly predicted in 55% and 82% of cases, respectively (p=0.04). Biopsies underestimated ploidy in 9/20 tumors (45%) with heterogeneous ploidy status. Underestimation mainly occurred when one or two cores were analyzed. CONCLUSIONS: Preoperative prediction of the ploidy status of prostate cancer is hampered by tumor heterogeneity. Analysis of multiple biopsies is important for correct preoperative ploidy estimation. PMID: 16257840 [PubMed - indexed for MEDLINE]

Posted by at 8:08 PM |

February 12, 2006

Re: luteinizing hormone-releasing hormone agonist effects on skeletal muscle: how hormonal therapy in prostate cancer affects muscular strength.


Re: luteinizing hormone-releasing hormone agonist effects on skeletal muscle: how hormonal therapy in prostate cancer affects muscular strength.
Related Articles Re: luteinizing hormone-releasing hormone agonist effects on skeletal muscle: how hormonal therapy in prostate cancer affects muscular strength. J Urol. 2005 Nov;174(5):2068-9 Authors: Marcora S, Oliver S, Callow N, Lemmey A, Stuart N PMID: 16217402 [PubMed - indexed for MEDLINE]

Posted by at 4:08 PM |