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JAMA, Vol. 281, No. 17. (5 May 1999), pp. 1591-1597.CONTEXT: In men who develop an elevated serum prostate-specific antigen level (PSA) after having undergone a radical prostatectomy, the natural history of progression to distant metastases and death due to prostate cancer is unknown. OBJECTIVE: To characterize the time course of disease progression in men with biochemical recurrence after radical prostatectomy. DESIGN: A retrospective review of a large surgical series with median (SD) follow-up of 5.3 (3.7) years (range, 0.5-15 years) between April 1982 and April 1997. SETTING: An urban academic tertiary referral institution. PATIENTS: A total of 1997 men undergoing radical prostatectomy, by a single surgeon, for clinically localized prostate cancer. None received neoadjuvant therapy, and none had received adjuvant hormonal therapy prior to documented distant metastases. MAIN OUTCOME MEASURES: After surgery, men were followed up with PSA assays and digital rectal examinations every 3 months for the first year, semiannually for the second year, and annually thereafter. A detectable serum PSA level of at least 0.2 ng/mL was evidence of biochemical recurrence. Distant metastases were diagnosed by radionuclide bone scan, chest radiograph, or other body imaging, which was performed at the time of biochemical recurrence and annually thereafter. RESULTS: The actuarial metastasis-free survival for all 1997 men was 82% (95% confidence interval, 76%-88%) at 15 years after surgery. Of the 1997 men, 315 (15%) developed biochemical PSA level elevation. Eleven of these underwent early hormone therapy after the recurrence and are not included in the study. Of the remaining 304 men, 103 (34%) developed metastatic disease within the study period. The median actuarial time to metastases was 8 years from the time of PSA level elevation. In survival analysis, time to biochemical progression (P, citeulike.org

CA Cancer J Clin, Vol. 43, No. 1. (b 1993), pp. 7-26.CC Boring, TS Squires, T Tong, citeulike.org

Annu Rev Genomics Hum Genet, Vol. 5 (2004), pp. 151-175.Prostate cancer is a heterogeneous disease with multiple loci contributing to susceptibility. Traditionally, genome-wide scans using high-risk families have utilized stratification by number of affected individuals, family history of other cancers, or family age at diagnosis to improve genetic homogeneity. In addition to locus heterogeneity, for later onset diseases such as prostate cancer, a major limitation to mapping efforts is that key parental DNA samples are rarely available. The lack of available samples from upper generations reduces inheritance information, and as a result, the standard 10-cM genome scan does not provide full power to detect linkage. To increase the ability to find disease-associated loci, much denser genome-wide scans must be undertaken in multiple ethnic groups. In addition, new ways of defining homogenous subsets of families need to be developed.EA Ostrander, K Markianos, JL Stanford, citeulike.org

East African medical journal, Vol. 84, No. 9 Suppl. (September 2007)OBJECTIVE: To carry out an overview of prostate cancer in indigenous back Africans in sub-Saharan Africa and blacks of African ancestry in diaspora. DATA SOURCE: Review of all published literature on prostate cancer on indigenous black Africans and Africans in diaspora was carried out through medline and index medicus searches. DATA SELECTION: Published data of prostate cancer in indigenous black Africans and black men in diaspora from 1935-2007 were included in the review. DATA EXTRACTION: Abstracts of articles identified were assessed, read and analysed to determine their possible suitability and relevance to the title under review. DATA SYNTHESIS: After establishing relevance from the abstract, the entire paper was read, and the significant points included in the review. CONCLUSION: Prostate cancer incidence and magnitude in black Africans was grossly misunderstood and underestimated in the past. Prostate cancer incidence is on the increase and currently is perhaps the most common urological malignancy affecting black Africans. Its incidence and clinical characteristics is similar to that of the Africans in diaspora but different from all other races. There currently exists significant evidence which suggests a common enhancing genetic predisposition in black men to prostate cancer. There is very urgent need for further investigation of this phenomenon through randomised controlled multicentre studies involving indigenous black Africans and black men in diaspora.GA Magoha, citeulike.org

Clinical cancer research : an official journal of the American Association for Cancer Research, Vol. 14, No. 11. (1 June 2008), pp. 3254-3261.PURPOSE: Pathologic examination of prostate glands removed from patients with prostate cancer commonly reveals infiltrating CD4+ and CD8+ T cells. Little is known about the phenotype of these cells, despite accumulating evidence suggesting a potential role for chronic inflammation in the etiology of prostate cancer. EXPERIMENTAL DESIGN: We developed a technique that samples the majority of the peripheral prostate through serial needle aspirates. CD4+ prostate-infiltrating lymphocytes (PIL) were isolated using magnetic beads and analyzed for subset skewing using both flow cytometry and quantitative reverse transcription-PCR. The transcriptional profile of fluorescence-activated cell sorted prostate-infiltrating regulatory T cells (CD4+, CD25+, GITR+) was compared with naïve, peripheral blood T cells using microarray analysis. RESULTS: CD4+ PIL showed a paucity of TH2 (interleukin-4-secreting) cells, a surprising finding given the generally accepted association of these cells with chronic, smoldering inflammation. Instead, CD4+ PIL seemed to be skewed towards a regulatory Treg phenotype (FoxP3+) as well as towards the TH17 phenotype (interleukin-17+). We also found that a preponderance of TH17-mediated inflammation was associated with a lower pathologic Gleason score. These protein level data were reflected at the message level, as analyzed by quantitative reverse transcription-PCR. Microarray analysis of pooled prostate-infiltrating T(reg) revealed expected Treg-associated transcripts (FoxP3, CTLA-4, GITR, LAG-3) as well as a number of unique cell surface markers that may serve as additional Treg markers. CONCLUSION: Taken together, these data suggest that TH17 and/or Treg CD4+ T cells (rather than TH2 T cells) may be involved in the development or progression of prostate cancer.KS Sfanos, TC Bruno, CH Maris, L Xu, CJ Thoburn, AM DeMarzo, AK Meeker, WB Isaacs, CG Drake, citeulike.org

The Prostate, Vol. 45, No. 2. (2000), pp. 87-100.No abstract.Keith Griffiths, citeulike.org

BMC Genomics, Vol. 8 (26 January 2007), 32.Steven Quayle, Heidi Hare, Allen Delaney, Martin Hirst, Dorothy Hwang, Jacqueline Schein, Steven Jones, Marco Marra, Marianne Sadar, citeulike.org

Journal of Membrane Biology, Vol. 194, No. 3. (1 July 2003), pp. 187-197.Claudins are a family of proteins involved in forming tight junctions between cells. Here we describe two forms of claudin-7 (CLDN-7), a full-length form of CLDN-7 with 211 amino-acid residues and a C-terminal truncated form with 158 amino-acid residues. These two forms of CLDN-7 are able to regulate the expression of a tissue-specific protein, the prostate-specific antigen (PSA), in the LNCaP prostate cancer cell line. We also found that the expression of CLDN-7 is responsive to androgen stimulation in the LNCaP cell line, suggesting that this protein is involved in the regulatory mechanism of androgen. Both forms of claudin-7 are expressed in human prostate, kidney and lung samples, and in most samples, the full-length form of claudin-7 was predominant. However, in some prostate samples from healthy individuals, the truncated form of claudin-7 is predominantly expressed. Our results demonstrated that unlike other claudins, CLDN-7 has both structural and regulatory functions, and the two forms of CLDN-7 may be related to cell differentiation in organ development.Zheng, D Yu, M Foroohar, E Ko, J Chan, N Kim, R Chiu, S Pang, citeulike.org

BMC Molecular Biology, Vol. 8 (21 March 2007), 25.Dagmar Kube, Dilara Savci-Heijink, Anne-Francoise Lamblin, Farhad Kosari, George Vasmatzis, John Cheville, Donald Connelly, George Klee, citeulike.org

BMC Urology, Vol. 7 (02 March 2007), 3.Marc Dall'era, Lawrence True, Andrew Siegel, Michael Porter, Tracy Sherertz, Alvin Liu, citeulike.org