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We hypothesized that soy phytochemicals may have immunomodulatory properties that may affect prostate carcinogenesis and progression. A randomized, phase II trial was conducted in 32 patients with prostate cancer with asymptomatic biochemical recurrence but no measurable disease on standard staging studies. Patients were randomized to two slices of soy bread (34 mg isoflavones/slice) or soy bread containing almond powder daily as a source of β-glucosidase. Flow cytometry and bioplex assays were used to measure cytokines or immune cell phenotype in blood at baseline (day 0) and following intervention (day 56). Adequate blood samples were available at enrollment and day 56 and evaluated. Multiple plasma cytokines and chemokines were significantly decreased on day 56 versus baseline. Subgroup analysis indicated reduced TH1 (P = 0.028) and myeloid-derived suppressor cell (MDSC)-associated cytokines (P = 0.035). TH2 and TH17 cytokines were not significantly altered. Phenotypic analysis revealed no change in CD8+ or CD4+ T cells but showed increased CD56+ natural killer (NK) cells (P = 0.038). The percentage of cells with a T regulatory cell phenotype (CD4+CD25+FoxP3+) was significantly decreased after 56 days of soy bread (P = 0.0136). Significantly decreased monocytic (CD33+HLADRnegCD14+) MDSC were observed in patients consuming soy bread (P = 0.0056). These data suggest that soy bread modulates systemic soluble and cellular biomarkers consistent with limiting inflammation and suppression of MDSCs. Additional studies to elucidate impact on the carcinogenic process or as a complement to immune-based therapy are required. Cancer Prev Res; 8(11); 1036–44. ©2015 AACR.

Supplemental Data Table 2A and 2B to describe changes in cytokine and cellular biomarkers between soy and soy-almond bread.

Mean Differences in Cytokines.

Carotenoids are a diverse family of phytochemicals with over 1000 different carotenoids present in nature. A human diet containing a variety of plant foods typically includes approximately 50 different carotenoids, although six (α-carotene, β-carotene, β-cryptoxanthin, lycopene, lutein, and zeaxanthin) comprise over 90% of total carotenoid intake. Most carotenoids do not meet the definition of a nutrient, but several can be cleaved to form vitamin A and are important contributors to vitamin A nutriture and prevention of vitamin A deficiency. Large epidemiologic studies suggest that diets rich in total or specific carotenoids are associated with a reduced risk of several diseases including various types of cancer, cardiovascular disease, cognitive disorders, and age-related macular degeneration. However, accurate measurement of dietary intake is challenging and current methods of dietary assessment, including food frequency questionnaires, diet records and 24-h recalls, have strengths and limitations regarding estimating carotenoid intake. Additionally, carotenoid bioavailability from the diet is influenced by many variables including food processing and cooking, meal composition, and individual characteristics of the host including age, digestive efficiency, nutritional status and genetic polymorphisms. Carotenoids are deposited in many human tissues and can be measured using a variety of techniques including high performance liquid chromatography (HPLC) and mass spectrometry (MS). Continued research is necessary to improve dietary intake assessment and establish biologically relevant dose-response relationships in the context of individual variability to advance our understanding of diet, disease risk, and health promotion.