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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.


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]


(((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.


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]


(((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.


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]


(((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.


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]


(((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.


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]


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]


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]


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]


(((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.


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]


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]


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]


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]


(((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.


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]


(((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.


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]

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]

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]

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]

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]

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]

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]

(((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
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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]

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]

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]

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]

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]

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]

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]

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]

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]

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]

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]

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]

Targeting apoptosis in prostate cancer: focus on caspases and inhibitors of apoptosis proteins.


Targeting apoptosis in prostate cancer: focus on caspases and inhibitors of apoptosis proteins.
Related Articles Targeting apoptosis in prostate cancer: focus on caspases and inhibitors of apoptosis proteins. BJU Int. 2005 Dec;96 Suppl 2:30-4 Authors: Watson RW, Fitzpatrick JM Androgens are critical to the growth and differentiation of prostate epithelial cells. Removal of androgen normally results in apoptosis, but androgen-independent tumours have developed mechanisms that allow cells to survive the loss of androgen. The caspases are central mediators of cell death. An important area for research involves manipulating caspases by novel mechanisms to induce apoptosis. However, such mechanisms as diethylmaleate priming are limited by an inability to selectively target tumour cells. Inhibitors of apoptosis proteins (IAPs) are recently identified anti-apoptotic caspase regulators. Each IAP homologue has a different mechanism of action. Because more than one member of the IAP family may be overexpressed in prostate cancer, successful treatment strategies will be defined by the ability to block all of the IAP expressed. Anti-sense oligonucleotide strategies have been shown to decrease IAP expression and increase prostate cancer cell susceptibility to apoptotic induction, although not by mitochondrial-mediated pathways. Fully understanding the basic apoptotic pathway and its regulation in prostate cancer will lead to more targets for manipulation, which can be translated into novel therapies. This article focuses on the role of the caspases and IAP in developing a rational approach to using apoptosis as a therapeutic target. PMID: 16359436 [PubMed - indexed for MEDLINE]

February 9, 2006

Acute renal failure secondary to imatinib mesylate treatment in prostate cancer.


Acute renal failure secondary to imatinib mesylate treatment in prostate cancer.
Related Articles Acute renal failure secondary to imatinib mesylate treatment in prostate cancer. Ann Pharmacother. 2005 Dec;39(12):2136-8 Authors: Foringer JR, Verani RR, Tjia VM, Finkel KW, Samuels JA, Guntupalli JS OBJECTIVE: To report a case of acute renal failure associated with the administration of imatinib mesylate. CASE SUMMARY: A 64-year-old man diagnosed with prostate cancer was enrolled in a Phase I trial of imatinib mesylate plus taxotere on a protocol that required a run-in period of imatinib mesylate alone. During therapy with imatinib mesylate, the patient developed acute renal failure, requiring hemodialysis. A renal biopsy revealed tubular vacuolization. Renal failure resolved with cessation of imatinib mesylate. DISCUSSION: Imatinib mesylate is a protein tyrosine kinase inhibitor that inhibits the BCR-ABL tyrosine kinase, the receptor tyrosine kinases for platelet-derived growth factor, and stem cell factor c-kit. Prostate cancer has been identified as a target for therapy with imatinib mesylate. This patient had no other confounding factors for the cause of the renal failure. An objective causality assessment determined that imatinib mesylate was the probable cause of the acute renal failure. The presence of a primary glomerular disease was excluded by biopsy. CONCLUSIONS: Imatinib mesylate-induced acute renal failure has now been linked to toxic effects on renal tubular cells in 3 cases. Renal function should be closely monitored during imatinib mesylate therapy. PMID: 16288076 [PubMed - in process]

Evaluation of human fetal bone implants in SCID mice as a model of prostate cancer bone metastasis.


Evaluation of human fetal bone implants in SCID mice as a model of prostate cancer bone metastasis.
Related Articles Evaluation of human fetal bone implants in SCID mice as a model of prostate cancer bone metastasis. Oncol Rep. 2006 Mar;15(3):519-24 Authors: Singh AS, Macpherson GR, Price DK, Schimel D, Figg WD The metastasis of prostate cancer cells to the bone marrow constitutes the major source of morbidity and mortality in prostate cancer. Studying this process has been hampered by the lack of preclinical models to evaluate novel therapeutics and to study the biology of the disease. One proposed model utilizes human fetal bone implants to serve as the target for prostate cancer cells injected via the tail vein. We employed this model to test the ability of zoledronic acid to prophylax and to treat bone metastases. To improve the rate of bone metastasis, we used two bone implants instead of one to evaluate the cell lines PC3 and PC3M, a more metastatic subline. For this purpose we generated the novel cell line PC3EGFPLuc, which can be used for luminescence and/or fluorescence imaging in vivo. We did not observe bone implant metastases in 52 mice, with 90 bone implants following tail vein injection of 1x10(6) PC3 or PC3M cells. Soft tissue lesions in the buttocks and hind limbs as well as cellular growth in the hindlimbs were observed via bioluminescence imaging. This evidence together with literature findings suggests that this model produces artifactual 'bone metastasis' lesions. PMID: 16465406 [PubMed - in process]

February 8, 2006

Long-term clinical outcomes of 420 consecutive prostate cancer patients in a single institute.


Long-term clinical outcomes of 420 consecutive prostate cancer patients in a single institute.
Related Articles Long-term clinical outcomes of 420 consecutive prostate cancer patients in a single institute. Acta Med Okayama. 2005 Oct;59(5):195-9 Authors: Edamura K, Saika T, Senoh T, Koizumi F, Manabe D, Ebara S, Kaku H, Yokoyama T, Abarzua F, Nagai A, Nasu Y, Tsushima T, Kumon H This study was undertaken to reveal the trends of prostate cancer and the outcome of treatment modalities for each disease stage in patients in a single institute over a 10-year period. From January 1994 through December 2003, 420 consecutive patients with previously untreated and histologically confirmed prostate cancer were analyzed for annual distributions of disease stages and treatment modalities and for long-term clinical progression-free survival, prostate cancer-specific survival, and prostate-specific antigen (PSA) failure-free survival rates for each stage and treatment modality. Annual trends showed that the number of patients, especially those with clinically localized cancer, increased dramatically. The 5-year disease-specific survival rates for patients with clinically localized disease were 100 percent for all treatment modalities, including hormonal therapy alone. Patients with PSA levels less than 10 ng/ml showed an 81 percent 5-year PSA failure-free survival rate with radical prostatectomy. Stage C patients treated by surgery or radiation-based therapy with concomitant hormonal therapy obtained 93 percent and 100 percent cause-specific survival rates, respectively, and those treated by hormonal therapy alone showed a 79 percent rate. The number of patients with localized prostate cancer was increasing in this decade. While long-term hormonal therapy alone was highly efficient in controlling localized prostate cancer, radical therapies in conjunction with neo-adjuvant hormonal therapy produced better survival rates in cases of locally advanced disease. PMID: 16286958 [PubMed - in process]

Laparoscopic surgery for melanoma metastases to the adrenal gland.


Laparoscopic surgery for melanoma metastases to the adrenal gland.
Related Articles Laparoscopic surgery for melanoma metastases to the adrenal gland. Expert Rev Anticancer Ther. 2004 Oct;4(5):837-41 Authors: Sturgeon C, Leong SP, Duh QY The probability of developing cutaneous melanoma is now predicted to be one in 55 for males and one in 88 for females. Although melanoma is relatively uncommon compared with other malignancies such as breast (one in seven) or prostate cancer (one in six), the incidence is growing at an alarming rate. The development of novel strategies for the management of advanced disease will become even more urgent and require continued and controlled investigations over the next 10 years. Surgery is effective for the palliation of isolated resectable metastases. However, most patients with Stage IV melanoma have widespread disease and are not cured by metastasectomy. For the few individuals with isolated adrenal metastases from melanoma, complete resection appears to confer a survival advantage. New data are emerging about the efficacy and outcome of laparoscopic adrenalectomy for malignant lesions. However, the natural history of laparoscopic surgery for these lesions is still unknown. The indications for and limitations of laparoscopic adrenalectomy for metastatic melanoma are discussed. PMID: 15485317 [PubMed - indexed for MEDLINE]

February 7, 2006

Correlation between LUTS (AUA-SS) and erectile dysfunction (SHIM) in an age-matched racially diverse male population: data from the prostate cancer awareness week (PCAW).


Correlation between LUTS (AUA-SS) and erectile dysfunction (SHIM) in an age-matched racially diverse male population: data from the prostate cancer awareness week (PCAW).
Related Articles Correlation between LUTS (AUA-SS) and erectile dysfunction (SHIM) in an age-matched racially diverse male population: data from the prostate cancer awareness week (PCAW). J Urol. 2005 Nov;174(5):1940 Authors: Seftel A PMID: 16217355 [PubMed - indexed for MEDLINE]

Cancer map patterns are they random or not?


Cancer map patterns are they random or not?
Related Articles Cancer map patterns are they random or not? Am J Prev Med. 2006 Feb;30(Suppl 2):S37-49 Authors: Kulldorff M, Song C, Gregorio D, Samociuk H, Dechello L BACKGROUND: Maps depicting the geographic variation in cancer incidence, mortality or treatment can be useful tools for developing cancer control and prevention programs, as well as for generating etiologic hypotheses. An important question with every cancer map is whether the geographic pattern seen is due to random fluctuations, as by pure chance there are always some areas with more cases than expected, or whether the map reflects true underlying geographic variation in screening, treatment practices, or etiologic risk factors. METHODS: Nine different tests for spatial randomness are evaluated in very practical settings by applying them to cancer maps for different types of data at different scales of spatial resolution: breast, prostate, and thyroid cancer incidence; breast cancer treatment and prostate cancer stage in Connecticut; and nasopharynx and prostate cancer mortality in the U.S. RESULTS: Tango's MEET, Oden's Ipop, and the spatial scan statistic performed well across all the data sets. Besag-Newell's R, Cuzick-Edwards k-NN, and Turnbull's CEPP often perform well, but the results are highly dependent on the parameter chosen. Moran's I performs poorly for most data sets, whereas Swartz Entropy Test and Whittemore's Test perform well for some data sets but not for other. CONCLUSIONS: When publishing cancer maps we recommend evaluating the spatial patterns observed using Tango's MEET, a global clustering test, and the spatial scan statistic, a cluster detection test. PMID: 16458789 [PubMed - in process]

February 5, 2006

Positive Inter-Regulation between beta-Catenin/T Cell Factor-4 Signaling and Endothelin-1 Signaling Potentiates Proliferation and Survival of Prostate Cancer Cells.


Positive Inter-Regulation between beta-Catenin/T Cell Factor-4 Signaling and Endothelin-1 Signaling Potentiates Proliferation and Survival of Prostate Cancer Cells.
Related Articles Positive Inter-Regulation between beta-Catenin/T Cell Factor-4 Signaling and Endothelin-1 Signaling Potentiates Proliferation and Survival of Prostate Cancer Cells. Mol Pharmacol. 2006 Feb;69(2):520-31 Authors: Sun P, Xiong H, Kim TH, Ren B, Zhang Z Both malignant and normal prostate epithelial cells produce endothelin-1 (ET-1), a critical factor in prostate cancer (CaP) progression. beta-Catenin (beta-cat), a key component of the Wnt signaling pathway, is also implicated in CaP progression via beta-cat/T cell factor (Tcf) signaling. We recently demonstrated that beta-cat/Tcf-4 regulates transcription of ET-1 in colon cancer cells. In the present study, we found that Tcf-4 specifically bound to and activated the ET-1 promoter in vivo in human CaP cells and mouse prostate tissue. Expression of ET-1 in DU145 CaP cells was down-regulated by knocking down endogenous beta-cat or Tcf-4. Ectopic activation of beta-cat/Tcf-4 signaling significantly elevated expression of ET-1 in LNCaP cells. In addition, genetic ablation of beta-cat significantly inhibited transcription of ET-1 in primary prostate epithelial cells. Meanwhile, exogenous ET-1 enhanced beta-cat/Tcf signaling and ET-1 expression in DU145 cells, which was blocked by both selective phosphatidylinositol 3-kinase (PI3K) inhibitor 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one (LY294002) and endothelin-A receptor antagonist cyclo(l-Leu-d-Trp-d-Asp-l-Pro-d-Val) (BQ123). Furthermore, knockdown of either beta-cat or Tcf-4 substantially reduced cell proliferation and potentiated paclitaxel-induced apoptosis in DU145 cells, which largely were rescued by treatment with exogenous ET-1. Together, our results suggest that beta-cat/Tcf-4 signaling transcriptionally activates ET-1 in CaP cells; meanwhile, ET-1 enhances beta-cat/Tcf-4 signaling and in turn further increases ET-1 expression in a PI3K-dependent manner. The positive inter-regulation between beta-cat/Tcf-4 signaling and ET-1 signaling potentiates proliferation and survival of CaP cells, thereby representing a novel mechanism that contributes to CaP progression. PMID: 16291872 [PubMed - in process]

[Nutrition and pharmacological treatment for prevention of prostate cancer]


[Nutrition and pharmacological treatment for prevention of prostate cancer]
Related Articles [Nutrition and pharmacological treatment for prevention of prostate cancer] Harefuah. 2006 Jan;145(1):47-51, 76-7 Authors: Segev Y, Nativ O Prostate cancer is the most common neoplasm and the second cause of cancer death. It is an excellent target for primary chemopreventive strategies for the following reasons: it is highly prevalent and has a long latency period, there are identifiable risk factors and a precursor lesion and it produces a biochemical marker (serum PSA) which can serve as an intermediate end point in chemoprevention studies. The goal of primary prevention strategies is to prevent development of clinical life-threatening neoplasms in asymptomatic patients with no evidence of clinical disease. Identification of populations at risk for developing cancer is the cornerstone of chemoprevention. Well-established risk factors for prostate cancer include African-American race, older age and family history. Data on diet and obesity are less clearly defined. Since high grade prostatic intraepithelial neoplasia (PIN) is an early predictor of prostate cancer, preventive strategies focusing on men with high grade PIN are being explored. It was demonstrated that finasteride could significantly reduce prostate cancer in asymptomatic men with normal PSA and no abnormalities on rectal examination. Elevated prostaglandin levels, and upregulation of cyclooxygenase-2 (COX-2) are found in prostate cancer cell lines. There is some epidemiologic evidence that regular use of NSAIDs, which inhibit COX-2, may be associated with a lower risk of prostate cancer. In the field of nutrition, data from prospective large-scale studies demonstrated that increased consumption of lycopene-rich tomato-based foods referred to a reduction in the risk for prostate cancer. Vitamin E was also found to reduce prostate cancer risk. Prospective data showed that vitamin D has an inhibitory effect on prostate cancer development while increased calcium consumption, independent from dietary intake, might increase the risk. Dietary fat intake, particularly from animal sources, may also increase the risk for prostate cancer. Whether this effect is strictly due to the already identified compounds or to other compounds, remains to be explored. Further study will hopefully help to establish a core set of nutritional and dietary factors that can positively or negatively affect prostate cancer development, as well as a set of pharmacologic agents that can reduce the risk of prostate cancer development and/or progression in selected patients. PMID: 16450727 [PubMed - in process]

January 30, 2006

Acute renal failure secondary to imatinib mesylate treatment in prostate cancer.


Acute renal failure secondary to imatinib mesylate treatment in prostate cancer.
Related Articles Acute renal failure secondary to imatinib mesylate treatment in prostate cancer. Ann Pharmacother. 2005 Dec;39(12):2136-8 Authors: Foringer JR, Verani RR, Tjia VM, Finkel KW, Samuels JA, Guntupalli JS OBJECTIVE: To report a case of acute renal failure associated with the administration of imatinib mesylate. CASE SUMMARY: A 64-year-old man diagnosed with prostate cancer was enrolled in a Phase I trial of imatinib mesylate plus taxotere on a protocol that required a run-in period of imatinib mesylate alone. During therapy with imatinib mesylate, the patient developed acute renal failure, requiring hemodialysis. A renal biopsy revealed tubular vacuolization. Renal failure resolved with cessation of imatinib mesylate. DISCUSSION: Imatinib mesylate is a protein tyrosine kinase inhibitor that inhibits the BCR-ABL tyrosine kinase, the receptor tyrosine kinases for platelet-derived growth factor, and stem cell factor c-kit. Prostate cancer has been identified as a target for therapy with imatinib mesylate. This patient had no other confounding factors for the cause of the renal failure. An objective causality assessment determined that imatinib mesylate was the probable cause of the acute renal failure. The presence of a primary glomerular disease was excluded by biopsy. CONCLUSIONS: Imatinib mesylate-induced acute renal failure has now been linked to toxic effects on renal tubular cells in 3 cases. Renal function should be closely monitored during imatinib mesylate therapy. PMID: 16288076 [PubMed - in process]

(((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])); +90 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])); +90 new citations
90 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 2006/01/28PubMed, 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.

January 29, 2006

Phase II trial of tesmilifene plus mitoxantrone and prednisone for hormone refractory prostate cancer: high subjective and objective response in patients with symptomatic metastases.


Phase II trial of tesmilifene plus mitoxantrone and prednisone for hormone refractory prostate cancer: high subjective and objective response in patients with symptomatic metastases.
Related Articles Phase II trial of tesmilifene plus mitoxantrone and prednisone for hormone refractory prostate cancer: high subjective and objective response in patients with symptomatic metastases. J Urol. 2005 Nov;174(5):1808-13; discussion 1813 Authors: Raghavan D, Brandes LJ, Klapp K, Snyder T, Styles E, Tsao-Wei D, Lieskovsky G, Quinn DI, Ramsey EW PURPOSE: Symptomatic, hormone refractory prostate cancer (HRCAP) is a major cause of morbidity with a median survival of less than 12 months and a 2-year survival of only up to 10% in most series. Mitoxantrone has been approved by the Food and Drug Administration for HRCAP. Preliminary data suggest that DPPE (N,N-diethyl-2-[4-(phenylmethyl) phenoxy]-ethanamine) or tesmilifene modulates cytotoxics to enhance the anticancer effect. In this phase II trial we assessed whether there is sufficient evidence of enhanced efficacy of DPPE and mitoxantrone to lead to a phase III clinical trial. MATERIALS AND METHODS: A total of 29 patients with a median age of 73 years, of whom 10% were older than 80 years, with progressive HRCAP received 5.3 mg/kg DPPE intravenously every 3 weeks, 12 mg/m mitoxantrone intravenously every weeks and 5 mg prednisone orally twice daily. All patients had pain at presentation, while 97% had bone metastases, 10% had liver metastases and 17% had lung metastases. Median prostate specific antigen (PSA) was 210 ng/ml (IQR 77 to 430). RESULTS: Of the patients 75% had some pain improvement, 66% had decreased analgesia, 59% had a PSA decrease of 50% or greater and 45% had a PSA decrease of 75% or greater. Actual (not actuarial) 2-year survival was 21%. CONCLUSIONS: Despite major limitations of historical comparison the PSA decrease and decreased symptoms with DPPE-mitoxantrone-prednisone compare favorably to those of mitoxantrone-prednisone and docetaxel-estramustine in the literature. The 2-year survival rate of 21% mandates further assessment. This will be tested in a phase III Southwest Oncology Group trial. PMID: 16217292 [PubMed - indexed for MEDLINE]

(((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])); +90 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])); +90 new citations
90 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 2006/01/28PubMed, 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.

January 28, 2006

The effect of percentage free prostate-specific antigen (PSA) level on the prostate cancer detection rate in a screening population with low PSA levels.


The effect of percentage free prostate-specific antigen (PSA) level on the prostate cancer detection rate in a screening population with low PSA levels.
Related Articles The effect of percentage free prostate-specific antigen (PSA) level on the prostate cancer detection rate in a screening population with low PSA levels. BJU Int. 2005 Nov;96(7):995-8 Authors: Pelzer AE, Volgger H, Bektic J, Berger AP, Rehder P, Bartsch G, Horninger W OBJECTIVE: To evaluate the prostate cancer detection rate at low total prostate-specific antigen (tPSA) ranges of 2.6-4 and 4.1-10 ng/mL, according to different percentage free (f/t) PSA levels in a screening population. SUBJECTS AND METHODS: In all, 1809 consecutive screening volunteers with a tPSA level of 2.6-10.0 ng/mL were assessed. Ten systematic ultrasonography-guided prostate biopsies and, since 2000, an additional five Doppler-enhanced targeted biopsies were taken on the basis of age-specific tPSA reference ranges. We analysed the detection rate of prostate cancer according to f/tPSA ranges of 0-9%, 10-14%, 15-18% and >18%. RESULTS: The detection rates for the subgroups with tPSA levels of 2.6-4.0 and 4.1-10.0 ng/mL were 20.2% and 27.0%, respectively. The cancer detection rate in the first group (2.6-4.0 ng/mL) at 0-10% fPSA was 22.9%, and that in the second group (4.1-10.0 ng/mL) at 0-10% was 36.9%. There were significant differences between these groups. If the f/tPSA was 10-15%, the cancer detection rate for the two groups were 22.6% and 32.5%, respectively (P < 0.05). There was no statistically significant difference in the cancer detecting rates at an f/tPSA of 15-18% or >18%. CONCLUSION: There is a statistically significantly higher cancer detection rate when the f/tPSA is <15% than in groups of men with a f/tPSA of >15% in screening population assessed primarily using tPSA level. PMID: 16225515 [PubMed - indexed for MEDLINE]

(((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])); +90 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])); +90 new citations
90 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 2006/01/28PubMed, 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.

January 24, 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]

Side-effects of treatments for locally advanced prostate cancer.


Side-effects of treatments for locally advanced prostate cancer.
Related Articles Side-effects of treatments for locally advanced prostate cancer. BJU Int. 2006 Jan;97(1):22-8 Authors: O'Connor KM, Fitzpatrick JM PMID: 16336322 [PubMed - indexed for MEDLINE]

January 23, 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. 2005 Nov 14; 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. (c) 2005 Wiley-Liss, Inc. PMID: 16287090 [PubMed - as supplied by publisher]

Pre-Treatment Nomogram for Disease-Specific Survival of Patients with Chemotherapy-Naive Androgen Independent Prostate Cancer.


Pre-Treatment Nomogram for Disease-Specific Survival of Patients with Chemotherapy-Naive Androgen Independent Prostate Cancer.
Related Articles Pre-Treatment Nomogram for Disease-Specific Survival of Patients with Chemotherapy-Naive Androgen Independent Prostate Cancer. Eur Urol. 2006 Jan 6; Authors: Svatek R, Karakiewicz PI, Shulman M, Karam J, Perrotte P, Benaim E OBJECTIVE: Our objective was to develop a nomogram that predicts the probability of cancer-specific survival in men with untreated androgen-independent prostate cancer (AIPC). METHODS: AIPC was diagnosed in 129 consecutive patients between 1989 and 2002. No patient received cytotoxic chemotherapy. Univariate and multivariate Cox regression models were used to test the association between prostate-specific antigen (PSA) level at initiation of androgen deprivation, PSA doubling time (PSADT), PSA nadir on androgen deprivation therapy (ADT), time from ADT to AIPC, and AIPC-specific mortality. Multivariate regression coefficients were then used to develop a nomogram predicting AIPC-specific survival at 12-60 mo after AIPC diagnosis. Two-hundred bootstrap resamples were used to internally validate the nomogram. RESULTS: AIPC-specific mortality was recorded in 74 of 129 patients (57.4%). Other-cause mortality was recorded in 7 men (5.4%). Median overall survival was 52.0 mo (mean, 36.0 mo) and median AIPC-specific survival was 54.0 mo (mean, 35.0 mo). In univariate regression models, all variables were significant predictors of AIPC-specific survival (p</=0.02). In multivariate models, PSADT and time from androgen deprivation to AIPC remained statistically significant (p</=0.004). Bootstrap-corrected predictive accuracy of the nomogram was 80.9% versus 74.9% for our previous model. CONCLUSIONS: A nomogram predicting AIPC-specific survival is between 13% and 14% more accurate than previous nomograms and 6% more accurate than tree regression-based predictions obtained from the same data. Moreover, a nomogram approach combines several advantages, such as user-friendly interface and precise estimation of individual recurrence probability at several time points after AIPC diagnosis, which all patients deserve to know and all treating physicians need to know. PMID: 16423446 [PubMed - as supplied by publisher]

January 21, 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]

Histopathological outcome in 167 patients operated on with radical retropubic prostatectomy.


Histopathological outcome in 167 patients operated on with radical retropubic prostatectomy.
Related Articles Histopathological outcome in 167 patients operated on with radical retropubic prostatectomy. Scand J Urol Nephrol. 2005;39(4):283-8 Authors: Solberg A, Viset T, Haugen OA, Mjønes J, Klepp O, Angelsen A OBJECTIVE: To evaluate the histopathological outcome in patients with prostate cancer operated on with radical retropubic prostatectomy. MATERIAL AND METHODS: A total of 167 patients with clinically organ-localized prostate cancer treated with open radical retropubic prostatectomy between 1996 and 2001 were divided into three equally sized consecutive cohorts (cohorts I-III). The prostatectomy specimens were re-examined by two pathologists with respect to pathological tumour stage, tumour grade and surgical tumour margins. RESULTS: The mean preoperative prostate-specific antigen (PSA) value was statistically significantly higher in cohort I compared to cohorts II and III: 13.2, 9.0 and 8.5 ng/ml, respectively (p<0.05). The incidence of locally advanced (pT3a-3b) tumours was 44% in cohort I and 20% in both cohorts II and III (p<0.05). The incidence of positive tumour margins was 58% in cohort I, compared to 30% in cohort II and 13% in cohort III (p<0.05). The incidence of positive intracapsular tumour margins was 55% in cohort I, compared to 25% in cohort II and 8.9% in cohort III (p<0.05). The incidence of positive tumour margins in the pT2 tumours in cohorts I-III was 57%, 26% and 8.9%, respectively (p<0.05). Cohort III had significantly more low-grade tumours (Gleason score 4-6; 58.9%) compared to cohorts I (31.5%) and II (34%). There was a higher incidence of Gleason score >or=7 in the pT3 tumours compared to the pT2 tumours (80% vs 46%) and in margin-positive compared to -negative tumours (69.6% vs 48.6%) (p<0.05). CONCLUSIONS: The decline in pT3 tumours and positive tumour margins between cohorts I-III is probably due to a gradually more strict selection of patients for radical retropubic prostatectomy. The successive reduction in positive intracapsular tumour margins is most likely due to an improved surgical technique. PMID: 16159748 [PubMed - indexed for MEDLINE]

January 18, 2006

Does docetaxel plus prednisone prolong the survival of men with metastatic hormone-refractory prostate cancer?


Does docetaxel plus prednisone prolong the survival of men with metastatic hormone-refractory prostate cancer?
Related Articles Does docetaxel plus prednisone prolong the survival of men with metastatic hormone-refractory prostate cancer? Nat Clin Pract Oncol. 2005 Feb;2(2):68-9 Authors: Protheroe A PMID: 16264873 [PubMed - indexed for MEDLINE]

Down-regulation of cyclooxygenase-2 and telomerase activity by beta-lapachone in human prostate carcinoma cells.


Down-regulation of cyclooxygenase-2 and telomerase activity by beta-lapachone in human prostate carcinoma cells.
Related Articles Down-regulation of cyclooxygenase-2 and telomerase activity by beta-lapachone in human prostate carcinoma cells. Pharmacol Res. 2005 Jun;51(6):553-60 Authors: Lee JH, Cheong J, Park YM, Choi YH Beta-lapachone, the product of a tree Tabebuia avellanedae from South America, is known to exhibit various pharmacologic properties, the mechanisms of which are poorly understood. In the present study, we investigated further possible mechanisms by which beta-lapachone exerts its anti-proliferative action in cultured human prostate carcinoma DU145 cells. Exposure of DU145 cells to beta-lapachone resulted in growth inhibition and induction of apoptosis in a dose-dependent manner as measured by MTT assay, fluorescent microscopy, and flow-cytometry analysis. The increase in apoptosis was associated with a dose-dependent up-regulation in pro-apoptotic Bax expression, down-regulation of anti-apoptotic Bcl-2, and proteolytic activation of caspase-3 protease. We found beta-lapachone decreased the levels of cyclooxygenase (COX)-2 mRNA and protein expression without significant changes in the levels of COX-1, which was correlated with a decrease in prostaglandin E2 (PGE2) synthesis. Furthermore, beta-lapachone treatment markedly inhibited the activity of telomerase in a dose-dependent fashion. Additionally, the expression of human telomerase reverse transcriptase (hTERT), a main determinant of the telomerase enzymatic activity, was progressively down-regulated by beta-lapachone treatment. Taken together, these findings provide important new insights into the possible molecular mechanisms of the anti-cancer activity of beta-lapachone. PMID: 15829436 [PubMed - indexed for MEDLINE]

January 13, 2006

Acute renal failure secondary to imatinib mesylate treatment in prostate cancer.


Acute renal failure secondary to imatinib mesylate treatment in prostate cancer.
Related Articles Acute renal failure secondary to imatinib mesylate treatment in prostate cancer. Ann Pharmacother. 2005 Dec;39(12):2136-8 Authors: Foringer JR, Verani RR, Tjia VM, Finkel KW, Samuels JA, Guntupalli JS OBJECTIVE: To report a case of acute renal failure associated with the administration of imatinib mesylate. CASE SUMMARY: A 64-year-old man diagnosed with prostate cancer was enrolled in a Phase I trial of imatinib mesylate plus taxotere on a protocol that required a run-in period of imatinib mesylate alone. During therapy with imatinib mesylate, the patient developed acute renal failure, requiring hemodialysis. A renal biopsy revealed tubular vacuolization. Renal failure resolved with cessation of imatinib mesylate. DISCUSSION: Imatinib mesylate is a protein tyrosine kinase inhibitor that inhibits the BCR-ABL tyrosine kinase, the receptor tyrosine kinases for platelet-derived growth factor, and stem cell factor c-kit. Prostate cancer has been identified as a target for therapy with imatinib mesylate. This patient had no other confounding factors for the cause of the renal failure. An objective causality assessment determined that imatinib mesylate was the probable cause of the acute renal failure. The presence of a primary glomerular disease was excluded by biopsy. CONCLUSIONS: Imatinib mesylate-induced acute renal failure has now been linked to toxic effects on renal tubular cells in 3 cases. Renal function should be closely monitored during imatinib mesylate therapy. PMID: 16288076 [PubMed - in process]

Time and PSA threshold model prognosticates long-term overall and disease-specific survival in prostate cancer patients as early as 3 months after external beam radiation therapy.


Time and PSA threshold model prognosticates long-term overall and disease-specific survival in prostate cancer patients as early as 3 months after external beam radiation therapy.
Related Articles Time and PSA threshold model prognosticates long-term overall and disease-specific survival in prostate cancer patients as early as 3 months after external beam radiation therapy. Prostate Cancer Prostatic Dis. 2005;8(4):353-8 Authors: Cavanaugh SX, Fuller CD, Kupelian PA, Reddy C, Bradshaw P, Pollock BH, Fuss M The specific aim of this analysis was to evaluate the capability of a time and prostate-specific antigen (PSA) threshold model to prognosticate overall survival (OS) and disease-specific survival (DSS) based on early PSA kinetics after radiotherapy for prostate cancer by retrospective review of outcomes in 918 patients. Crossing below analyzed PSA thresholds at specific defined time points reduced disease-specific death hazard ratios to relative to the cohort above threshold. The time and PSA threshold model demonstrates the ability to prognosticate OS and DSS as early as 3 months post-radiotherapy for prostate cancer. PMID: 16158079 [PubMed - indexed for MEDLINE]

January 12, 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]

January 11, 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]

Differences in clinical characteristics and disease-free survival for Latino, African American, and non-Latino white men with localized prostate cancer.


Differences in clinical characteristics and disease-free survival for Latino, African American, and non-Latino white men with localized prostate cancer.
Related Articles Differences in clinical characteristics and disease-free survival for Latino, African American, and non-Latino white men with localized prostate cancer. Cancer. 2006 Jan 6; Authors: Latini DM, Elkin EP, Cooperberg MR, Sadetsky N, Duchane J, Carroll PR BACKGROUND: Few studies of ethnicity and prostate cancer have included Latino men in analyses of baseline clinical characteristics, treatment selection, and disease-free survival (DFS). The present study examines the impact of Latino ethnicity on these parameters in a large, multiinstitutional database of men with prostate cancer. METHODS: We compared baseline disease characteristics and clinical outcomes for Latino (N = 138), non-Latino White (NLW, N = 5619), and African-American (AA, N = 608) men with localized prostate cancer by using chi-square and ANOVA for baseline variables and survival analysis to examine differences in time to recurrence. RESULTS: Latino men resembled AA men more than NLW on sociodemographic characteristics. AA men had higher Gleason scores and prostate-specific antigen (PSA) at diagnosis than Latino or NLW men (both P < 0.01). 10% of both Latino and AA men presented with advanced disease (T3b/T4/N+/M+) versus 4% of NLW (P < 0.01). Latino men did not receive different treatments than NLW or AA men after controlling for clinical and demographic factors; however, AA men were more likely to receive external beam radiation (OR = 1.51, 95% confidence interval [CI] = 0.99-2.31) and hormone treatment (OR = 1.56, 95% CI = 1.05-2.32) then NLW men. For prostatectomy patients, 3-year actuarial DFS rates were 83% for NLW men and 86% for Latino men versus 69% for AA men (P < 0.01). After controlling for clinical and sociodemographic variables, AA men were somewhat more likely than NLW to experience disease recurrence after radical prostatectomy (RP) (HR = 1.38, 95% CI = 0.98-1.94, P = 0.06). CONCLUSIONS: Latinos are more similar to African Americans on sociodemographic characteristics but more similar to NLW on clinical presentation, treatments received, and DFS. Cancer 2006. (c) 2006 American Cancer Society. PMID: 16400651 [PubMed - as supplied by publisher]

January 7, 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]

(((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])); +120 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])); +120 new citations
120 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 2006/01/07PubMed, 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.

Salvage radiotherapy for biochemical recurrence after radical prostatectomy.


Salvage radiotherapy for biochemical recurrence after radical prostatectomy.
Related Articles Salvage radiotherapy for biochemical recurrence after radical prostatectomy. BJU Int. 2005 Nov;96(7):1009-13 Authors: Terai A, Matsui Y, Yoshimura K, Arai Y, Dodo Y OBJECTIVE: To evaluate the clinical outcome of salvage radiotherapy (RT) for biochemical recurrence after radical prostatectomy (RP) at our institution. PATIENTS AND METHODS: Between March 1999 and January 2004, 37 patients had salvage RT for prostate-specific antigen (PSA) failure after RP, including eight who had had neoadjuvant hormone therapy. After surgery, PSA was measured with ultrasensitive immunoassays. In all patients RT was delivered to the prostatic bed at a total dose of 60 Gy with a four-field box technique. RESULTS: The median (range) PSA level before salvage RT was 0.146 (0.06-3.216) ng/mL and RT was started at a PSA level of <0.5 ng/mL in 34 of the 37 patients (92%). With a median follow-up of 31.9 (0-69.8), months, 11 patients (30%) had disease progression after RT and the 3- and 5-year progression-free probability was 74% and 54%, respectively. Univariate analysis showed that clinical and pathological tumour stages and PSA level before RT (>0.15 vs < or = 0.15 ng/mL) were significant predictors of disease progression. There were no late adverse events related to RT. CONCLUSION: Salvage RT for biochemical failure after RP at a low PSA level, using ultrasensitive immunoassays for monitoring, is a reasonably effective treatment. A relatively low radiation dose (60 Gy) seems to be effective. PMID: 16225518 [PubMed - indexed for MEDLINE]

(((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])); +120 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])); +120 new citations
120 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 2006/01/07PubMed, 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.

December 22, 2005

Can docetaxel plus estramustine prolong survival of men with metastatic


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]


Sleijfer S, Stoter G

Targeting apoptosis in prostate cancer: focus on caspases and inhibitors


Targeting apoptosis in prostate cancer: focus on caspases and inhibitors of apoptosis proteins.
Related Articles

Targeting apoptosis in prostate cancer: focus on caspases and inhibitors of apoptosis proteins.

BJU Int. 2005 Dec;96 Suppl 2:30-4

Authors: Watson RW, Fitzpatrick JM

Androgens are critical to the growth and differentiation of prostate epithelial cells. Removal of androgen normally results in apoptosis, but androgen-independent tumours have developed mechanisms that allow cells to survive the loss of androgen. The caspases are central mediators of cell death. An important area for research involves manipulating caspases by novel mechanisms to induce apoptosis. However, such mechanisms as diethylmaleate priming are limited by an inability to selectively target tumour cells. Inhibitors of apoptosis proteins (IAPs) are recently identified anti-apoptotic caspase regulators. Each IAP homologue has a different mechanism of action. Because more than one member of the IAP family may be overexpressed in prostate cancer, successful treatment strategies will be defined by the ability to block all of the IAP expressed. Anti-sense oligonucleotide strategies have been shown to decrease IAP expression and increase prostate cancer cell susceptibility to apoptotic induction, although not by mitochondrial-mediated pathways. Fully understanding the basic apoptotic pathway and its regulation in prostate cancer will lead to more targets for manipulation, which can be translated into novel therapies. This article focuses on the role of the caspases and IAP in developing a rational approach to using apoptosis as a therapeutic target.

PMID: 16359436 [PubMed - in process]


Watson RW, Fitzpatrick JM

December 19, 2005

Multidisciplinary treatment of synchronous primary rectal and prostate cancers. Related


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]


Colonias A, Farinash L, Miller L, Jones S, Medich DS, Greenberg L, Miller R, Parda DS

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


(((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])); +192 new citations

192 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 2005/12/19

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.


PubMed

December 12, 2005

Can docetaxel plus estramustine prolong survival of men with metastatic


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]


Sleijfer S, Stoter G

Effects of Histone Deacetylase Inhibitor (HDACi); Trichostatin-A (TSA) on the


Effects of Histone Deacetylase Inhibitor (HDACi); Trichostatin-A (TSA) on the expression of housekeeping genes.
Related Articles

Effects of Histone Deacetylase Inhibitor (HDACi); Trichostatin-A (TSA) on the expression of housekeeping genes.

Mol Cell Probes. 2005 Nov 30;

Authors: Mogal A, Abdulkadir SA

In quantitative RT-PCR (qRT-PCR), analysis of gene expression is dependent on normalization using housekeeping genes such as 18S rRNA, GAPDH and beta actin. However, variability in their expression has been reported to be caused by factors like drug treatment, pathological states and cell-cycle phase. An emerging area of cancer research focuses on identifying the role of epigenetic alterations such as histone modifications and DNA methylation in the initiation and progression of cancer. Histone acetylation is the best studied modification so far and has been probed through the use of histone deacetylase inhibitors (HDACi). Further, modulation of histone acetylation is currently being explored as a therapeutic strategy in the treatment of cancer and HDACis have shown promise in inhibiting tumorigenesis and metastasis. Trichostatin-A (TSA) is the most widely used HDACi. Therefore, we were driven to identify a suitable internal control for RT-PCR following TSA treatment. We performed quantitative RT-PCR analysis using mouse prostate tissue explants, human prostate cancer (LNCaP) cells and human breast cancer (T-47D and ZR-75-1) cells following TSA treatment. Expression of housekeeping genes including 18S rRNA, beta actin, GAPDH and ribosomal highly-basic 23-kDa protein (rb 23-kDa, RPL13A) were compared in vehicle versus TSA treated samples. Our results showed marked variations in 18S rRNA, beta actin mRNA and GAPDH mRNA levels in mouse prostate explants and a human prostate cancer (LNCaP) cell line following TSA treatment. Furthermore, in two human breast cancer cell lines (T-47D and ZR-75-1) 18S rRNA, beta actin mRNA and GAPDH mRNA levels varied significantly. However, RPL13A mRNA levels remained constant in all the conditions tested. Therefore, we recommend use of RPL13A as a standard for normalization during TSA treatment.

PMID: 16326072 [PubMed - as supplied by publisher]


Mogal A, Abdulkadir SA

December 8, 2005

High-affinity Near-infrared Fluorescent Small-molecule Contrast Agents for in vivo Imaging


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;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 - in process]


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

Open Retropubic Nerve-Sparing Radical Prostatectomy. Related Articles Open Retropubic Nerve-Sparing


Open Retropubic Nerve-Sparing Radical Prostatectomy.
Related Articles

Open Retropubic Nerve-Sparing Radical Prostatectomy.

Eur Urol. 2005 Nov 18;

Authors: Graefen M, Walz J, Huland H

Retropubic radical prostatectomy is the most commonly used therapeutic option for the treatment of clinically localized prostate cancer. An ongoing stage migration toward organ-confined cancers allows performance of a nerve-sparing procedure in a growing number of patients. Key elements for achieving convincing functional results are a sphincter-preserving ligation of the distal part of the Santorini plexus and the subtle preparation of the neurovascular bundle. This article gives a detailed description of the operative technique, which is demonstrated in the attached DVD. Furthermore, indication, oncologic outcome, and functional results addressing postoperative urinary continence and potency are discussed.

PMID: 16332409 [PubMed - as supplied by publisher]


Graefen M, Walz J, Huland H

December 3, 2005

Zoledronic acid is effective in preventing and delaying skeletal events


Zoledronic acid is effective in preventing and delaying skeletal events in patients with bone metastases secondary to genitourinary cancers.
Related Articles

Zoledronic acid is effective in preventing and delaying skeletal events in patients with bone metastases secondary to genitourinary cancers.

BJU Int. 2005 Nov;96(7):964-9

Authors: Saad F, Lipton A

Patients with metastatic bone disease often have severe bone pain and debilitating skeletal complications. Zoledronic acid is the only bisphosphonate shown to be safe and effective in reducing skeletal-related events (SREs), including pathological fractures, spinal cord compression, and radiation or surgery to bone in patients with bone metastases from advanced prostate cancer or renal cell carcinoma (RCC). In both tumour types, zoledronic acid significantly decreased the overall risk of developing an SRE, delayed their onset and significantly reduced the incidence of SREs compared with placebo. In patients with RCC, zoledronic acid also significantly delayed the time to progression of bone lesions by 5 months compared with placebo. Zoledronic acid is safe and well tolerated with long-term use.

PMID: 16225510 [PubMed - indexed for MEDLINE]


Saad F, Lipton A

December 1, 2005

Renal Safety and Efficacy of i.v. Bisphosphonates in Patients with


Renal Safety and Efficacy of i.v. Bisphosphonates in Patients with Skeletal Metastases Treated for up to 10 Years.
Related Articles

Renal Safety and Efficacy of i.v. Bisphosphonates in Patients with Skeletal Metastases Treated for up to 10 Years.

Oncologist. 2005 Nov;10(10):842-8

Authors: Guarneri V, Donati S, Nicolini M, Giovannelli S, D'Amico R, Conte PF

Introduction. Bisphosphonates (BPs) delay the onset or reduce the incidence of skeletal complications in patients with bone metastases. However, there are few data on the renal safety and activity of i.v. BPs beyond 2 years of administration.Materials and Methods. We retrospectively analyzed serum creatinine (SCr) levels and skeletal-related events (SREs) in cancer patients receiving i.v. BPs for >/= 24 months. All patients received 90 mg pamidronate every 3-4 weeks. Pre- and post-treatment SCr levels and the peak levels attained were recorded. A notable SCr increase was defined as: an increase >0.5 mg/dl for patients with baseline SCr <1.4 mg/dl; an increase >1 mg/dl for patients with baseline SCr >1.4 mg/dl; or doubling over baseline. The following parameters were also analyzed: the proportion of patients with at least one SRE, the distribution of each type of SRE, the time to first SRE, and the skeletal morbidity rate (SMR).Results. Fifty-seven patients with bone metastases resulting from breast cancer (BC) (n = 48), multiple myeloma (n = 7), renal cell carcinoma (n = 1), and prostate cancer (n = 1) were evaluated. The median age at the start of treatment was 57 years (range, 27-81); 25% of the patients were >70 years old. Forty-three patients received pamidronate then switched to zoledronic acid. The median overall duration of BP administration was 34 months (range, 24+ to 131+), with a median duration of zoledronic acid therapy of 25 months (range, 2-40). Twenty-seven of 48 BC patients received different chemotherapy regimens (median number of lines, 2; range, 1-6). The median SCr levels were: baseline, 0.82 mg/dl (range, 0.4-1.4); time of analysis, 0.89 mg/dl (0.4-2); highest level, 1.0 mg/dl (0.5-2). A notable SCr increase was observed in seven patients (12.2%; all grade 1). Twenty-six patients (45.6%) experienced SREs after starting BP treatment. The median time to first SRE was 911 days (95% confidence interval, 731; 1,023). The SMR was 0.20 events per year. Ten patients ceased treatment because of: an SCr level of 2 mg/dl (n = 1) physician decision (n = 6) and jaw osteonecrosis (n = 3). Ten patients died of progressive disease.Conclusion. i.v. BPs are safe and active during prolonged treatment administration, and renal function is maintained in patients receiving multiple cytotoxic therapies. Jaw osteonecrosis occurred in 5% of the study population, and its causal relationship with BP treatment requires further observation and study.

PMID: 16314295 [PubMed - in process]


Guarneri V, Donati S, Nicolini M, Giovannelli S, D'Amico R, Conte PF

November 29, 2005

[Therapy of hormone-refractory prostate cancer.] Related Articles [Therapy of hormone-refractory


[Therapy of hormone-refractory prostate cancer.]
Related Articles

[Therapy of hormone-refractory prostate cancer.]

Urologe A. 2005 Nov 26;

Authors: Heidenreich A

PSA-progression following primary ADT defines an androgen-refractory but still hormone sensitive PCA which might respond to secondary hormonal manipulations. Secondary hormonal manipulations will result in a PSA decline >50% in about 60-80% of the patients with a mean duration of 7-17 months depending on the type of treatment. PSA-progression following secondary endocrine treatment defines hormone-refractory prostate cancer (HRPCA) which might be treated by systemic chemotherapy. Based on the results of 2 prospective, randomized clinical phase-III trials comparing docetaxel and mitoxantrone, docetaxel results in a statistically significant survival benefit of 2.5 months, a significantly higher PSA- and pain response and represents the treatment of choice in the management of HRPCA. Bisphosphonates such as zoledronate represent another cornerstone in the management of PSA-progressive PCA demonstrating a significant benefit with regard to the prevention of skeletal related events. Furthermore, bisphosphonates might be indicated in the treatment of symptomatic bone pain. The current article critically reflects the various therapeutic options in the management of PSA progression following primary androgen deprivation for advanced prostate cancer.

PMID: 16311709 [PubMed - as supplied by publisher]


Heidenreich A

November 28, 2005

Non-genomic effects of the androgen receptor and Vitamin D agonist


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


Bonaccorsi L, Marchiani S, Ferruzzi P, Muratori M, Crescioli C, Forti G, Maggi M, Baldi E

20-year outcomes following conservative management of clinically localized prostate cancer


20-year outcomes following conservative management of clinically localized prostate cancer Albertsen PC, Hanley JA, Fine J, Division of Urology, University of Connecticut Health Center, Farmington, CT.
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20-year outcomes following conservative management of clinically localized prostate cancer Albertsen PC, Hanley JA, Fine J, Division of Urology, University of Connecticut Health Center, Farmington, CT.

Urol Oncol. 2005 Nov-Dec;23(6):459-60

Authors: Carroll PR

CONTEXT: The appropriate therapy for men with clinically localized prostate cancer is uncertain. A recent study suggested an increasing prostate cancer mortality rate for men who are alive more than 15 years following diagnosis. OBJECTIVE: To estimate 20-year survival based on a competing risk analysis of men who were diagnosed with clinically localized prostate cancer and treated with observation or androgen withdrawal therapy alone, stratified by age at diagnosis and histological findings. DESIGN, SETTING, AND PATIENTS: A retrospective population-based cohort study using Connecticut Tumor Registry data supplemented by hospital record and histology review of 767 men aged 55 to 74 years with clinically localized prostate cancer diagnosed between January 1, 1971, and December 31, 1984. Patients were treated with either observation or immediate or delayed androgen withdrawal therapy, with a median observation of 24 years. MAIN OUTCOME MEASURES: Probability of mortality from prostate cancer or other competing medical conditions, given a patient's age at diagnosis and tumor grade. RESULTS: The prostate cancer mortality rate was 33 per 1000 person-years during the first 15 years of follow-up (95% confidence interval [CI] 28-38) and 18 per 1000 person-years after 15 years of follow-up (95% CI 10-29). The mortality rates for these 2 follow-up periods were not statistically different, after adjusting for differences in tumor histology (rate ratio 1.1; 95% CI 0.6-1.9). Men with low-grade prostate cancers have a minimal risk of dying from prostate cancer during 20 years of follow-up (Gleason score of 2-4, 6 deaths per 1000 person-years; 95% CI 2-11). Men with high-grade prostate cancers have a high probability of dying from prostate cancer within 10 years of diagnosis (Gleason score of 8-10, 121 deaths per 1000 person-years; 95% CI 90-156). Men with Gleason score of 5 or 6 tumors have an intermediate risk of prostate cancer death. CONCLUSION: The annual mortality rate from prostate cancer appears to remain stable after 15 years from diagnosis, which does not support aggressive treatment for localized low-grade prostate cancer.

PMID: 16301129 [PubMed - in process]


Carroll PR

November 27, 2005

Pretreatment predictors of posttreatment PSA doubling times for patients undergoing


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


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

[In Process Citation] Related Articles [In Process Citation] Ann Urol


[In Process Citation]
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[In Process Citation]

Ann Urol (Paris). 2005 Oct;39 Suppl 3:S56-8

Authors: Bouchard P

Antagonists act by competitive inhibition of pituitary GnRH receptors for which they have a high affinity with a dose-dependent activity. The inhibition concerns LH but also FSH by inhibiting their secretion for 24 hours. At this time, only three molecules are available. Cetrorelix is mainly used for in vitro fertilization protocols, but research is currently being carried out in benign prostatic hypertrophy. Ganirelix is only used in medically assisted procreation. Abarelix is used in the United States as a monthly "depot" injection for the treatment of prostate cancer resistant to other therapies. Other molecules including orally active antagonists are in the course of clinical evaluation or in preclinical phases. The development of this therapeutic class is hampered by conflicting industrial interests and also by problems of tolerability in particular because of the side effects due to induced histamine release. The current indications in France are therefore limited to Assisted Reproductive Technology, and, recently, prostate cancer pending comparative studies versus agonists. The indications under development are endometriosis, myoma and precocious puberty, fields in which agonists have already been found to be effective. Male contraception seems to have a future however this therapeutic regimen remains very expensive. Finally, in benign prostatic hypertrophy, the antagonists administrated intermittently may be used to rapidly improve urinary flow.

PMID: 16302712 [PubMed - in process]


Bouchard P

November 20, 2005

Non-genomic effects of the androgen receptor and Vitamin D agonist


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


Bonaccorsi L, Marchiani S, Ferruzzi P, Muratori M, Crescioli C, Forti G, Maggi M, Baldi E

prostate cancer treatment; +70 new citations 70 new PubMed citations


prostate cancer treatment; +70 new citations

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

prostate cancer treatment

These PubMed results were generated on 2005/11/20

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.


PubMed

prostate cancer treatment; +70 new citations 70 new PubMed citations


prostate cancer treatment; +70 new citations

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

prostate cancer treatment

These PubMed results were generated on 2005/11/20

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.


PubMed

November 13, 2005

Does androgen deprivation improve treatment outcomes in patients with low-risk


Does androgen deprivation improve treatment outcomes in patients with low-risk and intermediate-risk prostate cancer?
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Does androgen deprivation improve treatment outcomes in patients with low-risk and intermediate-risk prostate cancer?

Nat Clin Pract Oncol. 2005 May;2(5):236-7

Authors: Miyamoto H, Messing EM, Chang C

PMID: 16264955 [PubMed - in process]


Miyamoto H, Messing EM, Chang C

Use of Complementary Therapies Among Breast and Prostate Cancer Patients


Use of Complementary Therapies Among Breast and Prostate Cancer Patients During Treatment: A Multisite Study.
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Use of Complementary Therapies Among Breast and Prostate Cancer Patients During Treatment: A Multisite Study.

Integr Cancer Ther. 2005 Dec;4(4):294-300

Authors: Hann DM, Baker F, Roberts CS, Witt C, McDonald J, Livingston M, Ruiterman J, Ampela R, Crammer C, Kaw O

PURPOSE: The purpose of this study was to compare the use of complementary therapies (CT) among breast and prostate cancer patients during active cancer treatment. The authors compared use and beliefs about the role of CT in cancer recovery. METHODS: A self-report survey was completed by 126 breast cancer patients and 82 prostate cancer patients as part of a multisite research project. The self-report questionnaire inquired about the use of various CTs, sources of information about CT, reasons for using CT, beliefs about the benefits and risks of CT, demographic characteristics, and cancer treatment history. RESULTS: Most of the respondents were older than 50 years, Caucasian, married, had attended or completed college, and were less than 1 year postdiagnosis. Prostate cancer patients were significantly older than the breast cancer patients (P < .001). Several differences emerged between the groups. Compared to the prostate cancer patients, significantly more of the breast cancer patients reported using CT because they wanted to reduce the risk of recurrence (P < .01), play a more active role in recovery (P < .01), help manage stress (P < .01), take a more holistic approach (P < .01), or boost the immune system (P < .01). More of the prostate cancer patients reported using CT to have more control of their recovery (P < .05). The 2 groups also differed significantly (P < .01) on several beliefs about the potential benefits and risks of using CT. CONCLUSIONS: Most of the patients in this study had used some form of CT since the time of their diagnosis. Differences among breast and prostate cancer patients with regard to their use of CT during cancer treatment should be considered by oncology professionals who are discussing this topic with their patients.

PMID: 16282506 [PubMed - as supplied by publisher]


Hann DM, Baker F, Roberts CS, Witt C, McDonald J, Livingston M, Ruiterman J, Ampela R, Crammer C, Kaw O