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These guidelines cover a wide range of topics from prostate cancer epidemiology to palliative care. Questions arising in daily clinical practice have been extracted and formulated as clinical questions. In the 4 years since the previous edition, there have been major changes -for example, robot-assisted prostatectomy has rapidly come into widespread use, and new hormones and anticancer drugs have been developed for castration-resistant prostate cancer. In response to these developments, the number of fields included in this guideline was increased from 11 in the 2012 edition to 16, and the number of clinical questions was increased from 63 to 70. The number of papers identified in searches of the existing literature increased from 4662 in the first edition, published in 2006, to 10 490 in the 2012 edition. The number of references has reached 29 448 just during this review period, indicating the exponential increase in research on the topic of prostate cancer. Clinical answers have been prepared based on the latest evidence. Recommendation grades for the clinical answers were determined by radiologists, pathologists, and other specialists in addition to urologists in order to reflect the recent advances and diversity of prostate cancer treatment. Here, we present a short English version of the original guideline, and overview its key clinical issues.

Study Type – Prognosis (case series)
Level of Evidence 4 OBJECTIVE To evaluate the clinical outcomes and histological types of renal cell carcinoma (RCC) arising in patients with end‐stage renal disease (ESRD), and to analyse the relationship of histopathological features with the duration of dialysis. PATIENTS AND METHODS Clinical characteristics and outcomes of 34 patients who had a radical nephrectomy for RCC arising in ESRD between November 1994 and June 2008 were investigated. Archive paraffin‐embedded tissue specimens obtained from 27 patients were histochemically and immunohistochemically analysed to determine the histopathological type. RESULTS There was one death from cancer and one patient with local progression within a median observation period of 29.5 months. Acquired cystic disease (ACD)‐associated RCC, clear cell‐papillary RCC, mucinous tubular and spindle‐cell carcinoma, and Xp11.2 translocation/TFE3 gene fusion were identified in eight, two, three and one patient, respectively. Conventional clear‐cell RCC was the predominant histological type (nine of 15) in patients with a duration of dialysis of <10 years, while ACD‐associated RCC was predominant (seven of 12) in those with dialysis for ≥10 years. Sarcomatoid foci were identified in three patients with dialysis for ≥10 years. Papillary adenoma was microscopically identified as a satellite tumour in 10 patients. CONCLUSION The spectrum of histological types of RCCs arising in ESRD is distinct from that of sporadic RCCs. Patients with a longer duration of dialysis should have particular attention for progression and metastasis. Immunohistochemical profiling is efficient in the histological classification of RCCs arising in ESRD, although knowledge about genetic changes remains to be accumulated.

months). Both enzymes were negatively expressed in PrECs andPrSCs at mRNA and protein levels. ATX expression was higher than AGK in AILNCaP, DU-145, and PC-3 cell-lines, while AGK was mainly expressed in LNCaP cells. Immunohistochemically, ATX and AGK expressions were negative in non-neoplastic epithelia, while both were weakly expressed in the majority of high-grade intra-epithelial neoplasia (HG-PIN). In cancer foci, ATX and AGK expressions were strong in 49% and 62%, weak in 40% and 32%, and negative in 11% and 6%, respectively. Expressions of both enzymes were significantly correlated with primary Gleason grade of cancer foci (P < 0.0001) and capsular invasion (P = 0.03 and 0.003 respectively). ATX expression was significantly correlated with probability of prostate specific antigen (PSA)-failure after surgery (P < 0.0001). In conclusion, LPA-producing enzymes (ATX and AGK) were frequently expressed in prostate cancer cells and precancerous HG-PIN. In particular, high expression levels of ATX were associated with both malignant potentials and poor outcomes. (Cancer Sci 2009; 100: 1631-1638) L ysophosphatidic acid (1-or 2-acyl-lysophosphatidic acid; LPA) is an extracellular bioactive phospholipid that mediates diverse biological activities including platelet aggregation, smooth muscle contraction, cancer cell proliferation, invasion, angiogenesis, and cytoskeletal reorganization.(1,2) This action is mediated by several interactive mechanisms: (a) It activates RhoA and NF-κβ genes inducing prostate cancer progression. (3,4) (b) It enhances SRE activity in promoters of immediate early growth-related genes.(5) (c) It stimulates secretion of polypeptide growth factors such as EGF (epidermal growth factor) and sensitizes cells to their growth promoting effects.(6,7) (d) Finally, LPA suppresses apoptosis of cancer cells by reducing levels of apoptosispromoting proteins. (8,9) We previously examined LPA activity in various biologic fluids and found a high LPA activity exerted by a specific type of its receptors (Edg-7/LPA3) in human seminal fluids.(10) Furthermore, addition of 18:1 LPA (oleoyl-LPA) to prostate epithelial and stromal cells resulted in up-regulation of a novel extracellular matrix signaling protein CYR-61, that has a growth stimulating potential. (11) Several routes are proposed for LPA production. It is produced extracellularly by lipoprotein oxidation through the action of secretory phospholipase A2 on microvesicles released from activated cells. (12) In plasma, it is produced by thrombin-activated platelets through the stimulated release of phospholipase-A1 and A2 (13) and lysophospholipase D (LysoPLD). (14,15) LysoPLD is identical to autotaxin (nucleotide pyrophosphatase phosphodiesterase-2; ATX/NPP2, EC 3.1.1.5), a cell motility-stimulating factor originally identified in the culture cell supernatant of malignant melanoma cells. (16,17) We previously found that human seminal fluids contain a large amount of ATX, which hydrolyses lysophosphatidylcholine to produce LPA.(18) While LPA signaling had ...