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Risk stratification of kidney cancer patients after nephrectomy may tailor surveillance intensity and selection for adjuvant therapy. Transcriptomic approaches are effective in predicting recurrence, but whether they add value to clinicopathologic models remains unclear.Data from patients with clear cell renal cell carcinoma (ccRCC) was downloaded from The Cancer Genome Atlas. Clinicopathologic variables were used to calculate SSIGN (stage, size, grade, and necrosis) scores. The 16 gene recurrence score (RS) signature was generated using RNA-seq data. Transcriptomic risk groups were calculated using the original thresholds. SSIGN groups were divided into low, intermediate, and high risk. Disease-free status was the primary endpoint assessed.SSIGN and RS were calculated for 428 patients with non-metastatic ccRCC. SSIGN low-, intermediate-, and high-risk groups demonstrated 2.7%, 15.2%, and 27.5%, 3-year recurrence risk, respectively. On multivariable analysis, the RS was associated with disease-free status (sub-distribution hazard ratio (sHR) 1.43 per 25 RS [95% CI (1.00-1.43)], p = 0.05). By risk groups, RS further risk stratified the SSIGN intermediate-risk group (sHR 2.22 [95% CI 1.10-4.50], p = 0.03). SSIGN intermediate-risk patients with low and high RS had a 3-year recurrence rate of 8.0% and 25.2%, respectively. Within this risk group, the area under the curve (AUC) at 3 years was 0.69 for SSIGN, 0.74 for RS, and 0.78 for their combination.Transcriptomic recurrence scores improve risk prediction even when controlling for clinicopathologic factors. Utility may be best suited for intermediate-risk patients who have heterogeneous outcomes and further refinement for clinical utility is warranted.

Immuno-oncology (IO) and targeted therapies, such as small molecule inhibitors, have changed the landscape of cancer treatment and prognosis; however, durable responses have been difficult to achieve due to tumor heterogeneity, development of drug resistance, and adverse effects that limit dosing and prolonged drug use. To improve upon the current medicinal armamentarium, there is an urgent need for new ways to understand, reverse, and treat carcinogenesis. Clustered regularly interspaced short palindromic repeats (CRISPR)-CRISPR-associated protein (Cas) 9 is a powerful and efficient tool for genome editing that has shown significant promise for developing new therapeutics. While CRISPR/Cas9 has been successfully used for pre-clinical cancer research, its use in the clinical setting is still in an early stage of development. The purpose of this review is to describe the CRISPR technology and to provide an overview of its current applications and future potential as cancer therapies.

The goal of this study was to assess the efficacy of the saw palmetto-based nutritional supplement, Prostataplex, for relieving the symptoms associated with benign prostatic hyperplasia (BPH) in men with mild to moderate degrees of BPH. A randomized, double-blind, placebo-controlled trial was performed in Shanghai, China. Eighty patients with BPH were randomly assigned to either the intervention group (39 cases) or control group (41 cases). Patients in the intervention group were administered Prostataplex orally and placebos were given to patients in the control group. The duration of treatment was 12 weeks in both groups. Following the intervention of Prostataplex, the maximum urinary flow rates (MFR), total scores of International Prostate Symptom Score (IPSS) and quality of life indicators were significantly better among the patients in the intervention group than those in the control group (P < 0.01 for all variables). Significant improvement of symptoms including dysuria, reducing nocturnal polyuria and increasing urinary flow rate was seen after two months of intervention, especially for the improvement of incomplete bladder emptying. Prostataplex has positive effects on improving symptoms as well as quality of life in men with mild to moderate BPH.

BACKGROUND Although cigarette smoking is considered a major risk factor for bladder carcinoma, little is known about the interaction between metabolic genes such as glutathione-S-transferase P1 and tobacco smoking in this process. GSTP1 may play a role in detoxification of tobacco-related carcinogens. METHODS In this case–control study of 145 cases with bladder carcinoma (male:female = 7.5:1) and 170 noncancer controls (male:female = 3.7:1), the relation between genetic polymorphisms of GSTP1 and susceptibility to bladder carcinoma was investigated and the gene–environment interaction between tobacco smoking and GSTP1 polymorphism was evaluated. Epidemiological data were collected for all cases and controls by a standard questionnaire. Polymorphisms of GSTP1 were measured by polymerase chain reaction–restriction fragment length polymorphism. The logistic regression model in SAS was used to estimate odds ratios (ORs) and 95% confidence intervals (95% CIs). RESULTS Cigarette smoking was confirmed as a risk factor of bladder carcinoma with an OR of 3.1 (95% CI: 1.7–5.9) after controlling for potential confounding factors. The OR for pack-years of smoking as a continuous variable was 2.4 (95% CI: 2.0–2.8). The ORs were 7.6 (95% CI: 1.18–49.51) for isoleucine/valine (Ile/Val) and 6.5 (95% CI: 1.01–41.56) for Ile/Ile when the homozygous Val/Val was considered as comparison group after adjusting for age, gender, race, and education. The adjusted OR for interaction between smoking and the GSTP1 (any Ile genotype) was 11.42 (95% CI: 0.53–248.15). CONCLUSIONS The results indicate that the Ile 105 allele is associated with an increased risk of bladder carcinoma and suggest that individuals who smoke and possess the Ile allele might be at increased risk for bladder carcinoma. Cancer 2005. © 2005 American Cancer Society.

Introduction: To investigate the accuracy of uroflowmetry with disposable QSingle compared to measurements with a home-based digital device and compared to a single clinical measurement. Patients and Methods: 60 men with lower urinary tract symptoms were included in a prospective, open-label, multicenter study. Uroflowmetry measurements were done using three devices/methods: single clinic-based method, followed by up to 12 measurements using the disposable home-based QSingle and up to 12 measurements using a home-based digital device. Subjective data on ease of use of QSingle and preference of patients was investigated and objective measures of Qmax and voided volume from the three devices were compared. Results: Mean Qmax values of 12, 13 and 16 ml/s were achieved with the QSingle device, standard clinic method, and digital device, respectively. Mean Qmax obtained with the QSingle device did not differ from that obtained with the clinic method. A significantly higher mean Qmax was recorded for the digital device. Mean voided volumes recorded with each device differed marginally. Handling capabilities of the QSingle device were considered good by all subjects. Conclusions: The accuracy of Qmax and voided volume mean measurements with QSingle was comparable to one standard clinic recording. QSingle offers a viable alternative to reduce the number of clinic visits and can be used by other caregivers.

Isolated prostate specific antigen (PSA) determinations in asymptomatic individuals have not demonstrated sufficient sensitivity and specificity to be useful in the routine evaluation of prostate disease. To enhance the accuracy of serum PSA we have used a quotient of serum PSA and prostate volume, which we refer to as prostate specific antigen density (PSAD). Prostate volume in this study was calculated from magnetic resonance imaging determinations of benign prostatic hypertrophy (BPH) or from the dimensions of the surgical specimen of cancer using the formula, length x width x depth x 0.5 = volume. A total of 61 patients with prostatic disease clinically confined to the prostate glands (41 with prostate cancer undergoing radical prostatectomy and 20 with BPH) was evaluated. The mean PSAD for prostate cancer was 0.581 while that for BPH was 0.044 (p less than 0.002). No patient with BPH had a PSAD of greater than 0.117 and only 1 patient had a density of 0.1 or greater. Of 34 patients with a PSAD of 0.1 or greater 33 had prostate cancer. Only 2 of the 41 prostate cancer patients and 14 of the BPH patients had a PSAD of 0.05 or less. There were 11 patients with a PSAD of greater than 0.05 and less than 0.1, including 6 with prostate cancer (1 with P0 disease) and 5 with BPH. Of the 6 prostate cancer patients 5 had a PSA of 4.0 or less and among the 5 patients with BPH 4 had a serum PSA of greater than 4.0 and 1 had a PSA of greater than 10. These results suggest that PSAD may be useful in distinguishing BPH and prostate cancer.