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Objective: To examine the role of several interrelated, potentially modifiable psychological factors (i.e., mindfulness and catastrophizing) in influencing patient-reported functioning. Methods: In this cross-sectional study, 107 patients with fibromyalgia completed self-report assessments of pain severity, functioning and impact of symptoms, mindfulness, and pain catastrophizing. Linear regression and bootstrapping mediation analyses were performed to assess the relationships between these factors. Results: Pain intensity was significantly and positively associated with pain catastrophizing and impact of fibromyalgia on functioning. Linear regression analyses indicated that pain intensity, catastrophizing, and mindfulness affect functioning in fibromyalgia. Follow-up mediation analysis revealed a significant indirect effect of pain catastrophizing on the relationship between pain intensity and fibromyalgia functioning. Conclusion: Individuals with fibromyalgia who have higher levels of pain and catastrophizing, and lower levels of mindfulness, are more likely to experience impaired functioning. Our findings suggest that pain catastrophizing appears to be an especially important variable contributing to reduced functioning in women with fibromyalgia. Therefore, catastrophizing-reducing treatments (e.g., cognitive behavioral therapy) are likely to have direct, beneficial impacts on functioning. [ABSTRACT FROM AUTHOR]

Engrailed variant-2 (EN2) has been suggested as a potential diagnostic biomarker; however, its presence and functional role in prostate cancer (PCa) cells is still controversial or unknown. Here, we analyzed 1) the expression/secretion profile of EN2 in five independent samples cohorts from PCa patients and controls (prostate tissues and/or urine) to determine its utility as a PCa biomarker; and 2) the functional role of EN2 in normal (RWPE1) and tumor (LNCaP/22Rv1/PC3) prostate cells to explore its potential value as therapeutic target. EN2 was overexpressed in our two cohorts of PCa tissues compared to control and in tumor cell lines compared with normal-like prostate cells. This profile was corroborated in silico in three independent data sets [The Cancer Genome Atlas(TCGA)/Memorial Sloan Kettering Cancer Center (MSKCC)/Grasso]. Consistently, urine EN2 levels were elevated and enabled discrimination between PCa and control patients. EN2 treatment increased cell proliferation in LNCaP/22Rv1/PC3 cells, migration in RWPE1/PC3 cells, and PSA secretion in LNCaP cells. These effects were associated, at least in the androgen-sensitive LNCaP cells, with increased AKT and androgen-receptor phosphorylation levels and with modulation of key cancer-associated genes. Consistently, EN2 treatment also regulated androgen-receptor activity (full-length and splicing variants) in androgen-sensitive 22Rv1 cells. Altogether, this study demonstrates the potential utility of EN2 as a non-invasive diagnostic biomarker for PCa and provides novel and valuable information to further investigate its putative utility to develop new therapeutic tools in PCa. [ABSTRACT FROM AUTHOR]