The effect of lycopene-containing foods in prostate cancer development remains undetermined. We tested whether a lycopene-rich tomato intervention could reduce the levels of prostate specific antigen (PSA) in prostate cancer patients. Prior to their curative treatment, 79 patients with prostate cancer were randomized to a nutritional intervention with either 1) tomato products containing 30 mg lycopene per day; 2) tomato products plus selenium, omega-3 fatty acids, soy isoflavones, grape/pomegranate juice, and green/black tea (tomato-plus); or 3) control diet for 3 weeks. The main analysis, which included patients in all risk categories, did not reveal differences in changes of PSA-values between the intervention and control groups. Post-hoc, exploratory analyses within intermediate risk (n = 41) patients based on tumor classification and Gleason score post-surgery, revealed that median PSA decreased significantly in the tomato group as compared to controls (-2.9% and +6.5% respectively, p = 0.016). In separate post-hoc analyses, we observed that median PSA-values decreased by 1% in patients with the highest increases in plasma lycopene, selenium and C20:5 n-3 fatty acid, compared to an 8.5% increase in the patients with the lowest increase in lycopene, selenium and C20:5 n-3 fatty acid (p = 0.003). Also, PSA decreased in patients with the highest increase in lycopene alone (p = 0.009). Three week nutritional interventions with tomato-products alone or in combination with selenium and n-3 fatty acids lower PSA in patients with non-metastatic prostate cancer. Our observation suggests that the effect may depend on both aggressiveness of the disease and the blood levels of lycopene, selenium and omega-3 fatty acids.

Recently, the Expanded Prostate Cancer Index Composite 26-item version (EPIC-26) was recommended for the assessment of adverse effects after the treatment of prostate cancer without clear reasons. This decision encouraged us to review the questionnaire development from the UCLA Prostate Cancer Index (UCLA-PCI) to the EPIC-16 CP with a focus on psychometric properties. We also reviewed PubMed for papers concerning such properties of the EPIC-26 since 2012 (latest review in 2011). Finally, we examined the psychometric properties of the EPIC-26 in a sample of Norwegian males treated with robot-assisted laparoscopic prostatectomy (RALP). This study used three methods: (1) Comparison of the content of the UCLA-PCI, EPIC-50, EPIC-26, and EPIC-16 CP; (2) Review of EPIC-26 and EPIC-16 CP papers in PubMed from 2012 to 2016, identifying papers reporting on the psychometric properties of these questionnaires; and (3) Psychometric examination of the EPIC-26 rating in 651 Norwegian men treated with RALP at a mean of 3.2 years post-surgery. The questionnaire development showed a significant increase in bother versus function items, and the EPIC-26 contains eight function and 18 bother items. Twelve papers concerning the EPIC-26 available on PubMed since 2012 support the psychometric properties of the EPIC-26. The Norwegian EPIC-26 findings supported the psychometric properties of the EPIC-26, but suggested six subdomains both by exploratory and confirmatory factor analyses. In general our examinations supported the adequate psychometric properties of the EPIC-26, although the factor structure, construct and predictive validity of the instrument should be examined further.

Prostate cancer is a common cause of cancer death in men. In advanced stages of prostate cancer, androgen deprivation therapy (ADT) is initiated. Despite ADT, prostate cancers invariably progress to become androgen independent. A growing body of evidence implicates iron dysmetabolism in prostate cancer progression. A bioactive peptide-rich salmon protein hydrolysate (SPH) has previously been demonstrated to modulate iron homeostatic mechanisms. In the present study, the anticancer effect of SPH and bicalutamide co-treatment on LNCaP and PC3 prostate cancer cell proliferation was investigated. Our results found that SPH potentiates the anti-proliferative effect of bicalutamide in a dose-dependent manner for both cell lines. In the presence of 160 µg/mL SPH, co-treatment with 1.0 µM bicalutamide decreased LNCaP cells’ relative colony survival from 25% (1.0 µM bicalutamide monotreatment) to 2% after culturing for 12 days. For PC3 cells, the relative colony survival diminished from 52% (10.0 µM bicalutamide) to 32% at an SPH concentration of 160 µg/mL. Gene expression profiling, employing quantitative real-time PCR, revealed that the inhibitory effects were related to significant FTH1 up-regulation with a concomitant TFRC down-regulation. In conclusion, our results provide in vitro evidence that SPH potentiates the growth inhibitory effect of bicalutamide on prostate cancer cells by modulating iron homeostasis mechanisms.