Purpose: The forkhead box transcription factor FoxP3 is specifically expressed in T cells with regulatory properties (Treg). Recently, high numbers of Treg were described to be associated with poor survival in different malignancies. The aim of the presented study was determine the prognostic effect of FoxP3 mRNA expression (reflecting the tissue content of Treg) in ovarian carcinoma and its relation with cytokines, such as IFN-g. Experimental Design: Total RNA was isolated from 99 ovarian carcinoma and from 14 healthy ovarian biopsies. Real-time PCR for FoxP3 was done and correlated with IFN-g-, CD3-, IRF-1-, SOCS-1-, HER-2-, and iNOS expression as well as patients'outcome.The mRNA data was corroborated by FoxP3 immunohistochemistry. Results: Quantitation of FoxP3 expression identified a patient subgroup (>81th percentile), which is characterized by a significantly worse prognosis in terms of overall survival (27.8 versus 77.3 months, P = 0.0034) and progression-free survival (18 versus 57.5 months; P = 0.0041). FoxP3 expression correlated with IFN-g, IRF-1, and CD3 expression. High FoxP3 expression represents an independent prognostic factor for overall survival (P = 0.004) and progression-free survival (P = 0.004). Conclusions: High expression levels of FoxP3 might represent a surrogate marker for an immunosuppressive milieu contributing to tumor immune escape. Strategies selectively depleting Treg might improve the antitumor activity of endogenously arising tumor-reactiveTcells and immunotherapies using vaccines or antibodies.Cancer patients can harbor significant numbers of CD8 and CD4 T cells specific for tumor antigens. In most cases, tumorreactive T cells fail to eradicate the tumor in vivo because they seem to be actively maintained in an unresponsive state. Several immune-evasion strategies of malignant tumors have been described thus far (reviewed in ref. 1). Recently, regulatory T cells (Treg), which are characterized by coexpression of CD4 and CD25, have also been attributed to contribute to cancer-related immunosuppression (2 -5). Treg represent 5% to 10% of total CD4 + T cells and are crucial for the repression of autoimmune disorders and transplant rejection (6). The activation of Treg is antigen specific; however, inhibition of CD4 + and CD8 + T cells seems to be antigen nonspecific. Very recent evidence showed that Treg abrogate CD8 + T cell -mediated tumor rejection in a transforming growth factor-h -dependent manner (7). The suggestion of a role for Treg in cancer-induced immunosuppression in humans arises from the observation that patients suffering from a variety of cancer types have an enlarged pool of Treg in the peripheral blood, tumor-draining lymph nodes, and in the tumor itself (8 -12). Exact characterization of Treg has been hampered by the lack of specific cell surface markers. The observation that autoimmune diseases occur in both humans and mice lacking functional FoxP3 (13) indicates that this transcription factor plays a crucial role in the regulation of Treg function. ...
OBJECTIVES To evaluate the relationship between clinical benign prostatic hyperplasia (BPH) and atherosclerosis, using colour Doppler ultrasonography (CDUS) and symptom scores. PATIENTS, SUBJECTS AND METHODS CDUS was used to evaluate prostatic vascularity in four groups of men, comprising young healthy subjects, patients presenting with coronary artery disease (CAD), diabetes mellitus, or peripheral arterial occlusive disease (PAOD). Resistive index (RI) measurements and computer‐assisted quantification of colour pixel density (CPD) were used to objectively evaluate perfusion. The International Prostate Symptom Score (IPSS) and the International Index of Erectile Function were used to quantify symptoms. RESULTS In diabetic patients and men with PAOD, perfusion of the transition zone (TZ) of the prostate was significantly lower (P < 0.001) and the RI of the TZ was significantly higher (P < 0.001) than in healthy controls and men with CAD. In diabetics and men with PAOD, the mean prostate volume was greater than in healthy controls and men with CAD. The IPSS in patients with vascular damage (diabetes, PAOD) was significantly worse than in the control group. CONCLUSIONS The significantly lower CPD and higher RI values of the TZ in patients with vascular disease than in healthy subjects support the hypothesis that an age‐related impairment of blood supply to the prostate has a key role in the development of BPH.
As results regarding associative demographic and disease-specific factors on health-related quality of life (HRQoL) in patients with multiple sclerosis (MS) are partially inconsistent and contradictory, we reinvestigated this question on a large Austrian MS dataset. Patients received a questionnaire covering demographic and disease-specific characteristics and the Nottingham health profile (NHP) for assessing HRQoL. In order to estimate the risk for suboptimal HRQoL, adjusted odds ratios were calculated from logistic regression models including gender, age, expanded disability status scale (EDSS), disease course, disease duration and walking ability as covariates. The EDSS was the only factor contributing to both physical and mental dimensions (P < 0.001), whereas disease course, gender and age showed a significant effect on all physical, but not consistently on mental dimensions. The regression models fitting better for physical than for mental dimensions, clearly indicate a lack of explanation of demographic and disease-specific factors in these dimensions of HRQoL.
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