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.

The use of immune checkpoint inhibitors to treat urothelial carcinoma (UC) is increasing rapidly without clear guidance for validated risk stratification. This multicenter retrospective study collected clinicopathological information on 463 patients, and 11 predefined variables were analyzed to develop a multivariate model predicting overall survival (OS). The model was validated using an independent dataset of 292 patients. Patient characteristics and outcomes were well balanced between the discovery and validation cohorts, which had median OS times of 10.2 and 12.5 mo, respectively. The final validated multivariate model was defined by risk scores based on the hazard ratios (HRs) of independent prognostic factors including performance status, site of metastasis, hemoglobin levels, and the neutrophil‐to‐lymphocyte ratio. The median OS times (95% confidence intervals [CIs]) for the low‐, intermediate‐, and high‐risk groups (discovery cohort) were not yet reached (NYR) (NYR–19.1), 6.8 mo (5.8‐8.9), and 2.3 mo (1.2‐2.6), respectively. The HRs (95% CI) for OS in the low‐ and intermediate‐risk groups vs the high‐risk group were 0.07 (0.04‐0.11) and 0.23 (0.15‐0.37), respectively. The objective response rates for in the low‐, intermediate‐, and high‐risk groups were 48.3%, 28.8%, and 10.5%, respectively. These differential outcomes were well reproduced in the validation cohort and in patients who received pembrolizumab after perioperative or first‐line chemotherapy (N = 584). In conclusion, the present study developed and validated a simple prognostic model predicting the oncological outcomes of pembrolizumab‐treated patients with chemoresistant UC. The model provides useful information for external validation, patient counseling, and clinical trial design.

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EPCA seems to reflect nuclear matrix alterations that occur in the earlier stage of prostate carcinogenesis. Individuals in whom the prostate is influenced by this field effect may be detected with this new biomarker.

Cancer stem cells are capable of transformation after apoptosis through the blebbishield emergency program. Reactive oxygen species (ROS) play an essential role in transformation. Understanding how ROS are linked to blebbishield-mediated transformation is necessary to develop efficient therapeutics that target the resurrection of cancer stem cells. Here we demonstrate that a novel PKC-ζ to p47phox interaction is required for ROS production in cancer cells. The combined use of the S6K inhibitor BI-D1870 with TNF-α inhibited the PKC-ζ to p47phox interaction, inhibited ROS production, degraded PKC-ζ, and activated caspases-3 and -8 to block transformation from blebbishields. BI-D1870 also inhibited transformation from cycloheximide-generated blebbishields. Thus ROS and the PKC-ζ to p47phox interaction are valid therapeutic targets to block transformation from blebbishields.