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San Giovanni Valdarno, Italy

Fredolini C.,S. Giovanni Bosco Hospital | Fredolini C.,University of Turin | Fredolini C.,George Mason University | Liotta L.A.,George Mason University | Petricoin E.F.,George Mason University
Critical Reviews in Clinical Laboratory Sciences | Year: 2010

Prostate cancer affects 3 in 10 men over the age of 50 years, and, unfortunately, the clinical course of the disease is poorly predicted. At present, there is no means that can distinguish indolent from aggressive/metastatic tumors. Thus, a personalized clinical approach could be helpful in diagnosing clinically relevant disease and guiding appropriate patient therapy. Individualized medicine requires a deep knowledge of the molecular mechanisms underpinning prostate cancer carcinogenesis. Proteomics may be the most powerful way to uncover biomarkers of detection, prognosis, and prediction, as proteins do the work of the cell and represent the majority of the diagnostic markers and drug targets today. Proteomic technologies are rapidly advancing beyond the two-dimensional gel separation techniques of the past to new types of mass spectrometry and protein microarray analyses. Biological fluids and tissue-cell proteomes from men with prostate cancer are being explored to identify diagnostic and prognostic biomarkers and therapeutic targets using these new proteomic approaches. Traditional and novel proteomic technology and their application to prostate cancer studies in translational research will be presented and discussed in this review. Proteomics coupled with powerful nanotechnology-based biomarker discovery approaches may provide a new and exciting opportunity for body fluid-borne biomarker discovery and characterization. While innovative mass spectrometry technology and nanotrap could be applied to improve the discovery and measurement of biomarkers for the early detection of prostate cancer, the use of tissue proteomic tools such as the reverse-phase protein microarray may provide new approaches for personalization of therapies tailored to each tumor's unique pathway activation network. © 2010 Informa Healthcare USA, Inc. Source


Coppola V.,Oncology and Molecular Medicine | Musumeci M.,Oncology and Molecular Medicine | Patrizii M.,Oncology and Molecular Medicine | Cannistraci A.,Oncology and Molecular Medicine | And 12 more authors.
Oncogene | Year: 2013

Prostate cancer is one of the leading causes of cancer-related death in men. Despite significant advances in prostate cancer diagnosis and management, the molecular events involved in the transformation of normal prostate cells into cancer cells have not been fully understood. It is generally accepted that prostate cancer derives from the basal compartment while expressing luminal markers. We investigated whether downregulation of the basal protein B-cell translocation gene 2 (BTG2) is implicated in prostate cancer transformation and progression. Here we show that BTG2 loss can shift normal prostate basal cells towards luminal markers expression, a phenotype also accompanied by the appearance of epithelial-mesenchymal transition (EMT) traits. We also show that the overexpression of microRNA (miR)-21 suppresses BTG2 levels and promotes the acquisition of luminal markers and EMT in prostate cells. Furthermore, by using an innovative lentiviral vector able to compete with endogenous mRNA through the overexpression of the 3′-untranslated region of BTG2, we demonstrate that in prostate tumor cells, the levels of luminal and EMT markers can be reduced by derepression of BTG2 from microRNA-mediated control. Finally, we show that the loss of BTG2 expression confers to non-tumorigenic prostate cells ability to grow in an orthotopic murine model, thus demonstrating the central role of BTG2 downregulaton in prostate cancer biology. © 2013 Macmillan Publishers Limited. All rights reserved. Source


Cozzolino M.,University of Milan | Brancaccio D.,Dialysis Unit | Cannella G.,San Martino Hospital | Messa P.,Policlinico Hospital | And 8 more authors.
Nephrology Dialysis Transplantation | Year: 2012

Background. Chronic kidney disease (CKD) patients affected by mineral bone disorders (MBD) have higher rates of all-cause and cardiovascular-related mortality. Approximately, one-third of dialysis patients have low serum parathyroid hormone (PTH) levels (≤150 pg/mL). However, the reason why these patients have higher mortality compared to patients with normal PTH levels has not yet been fully elucidated. Methods. The FARO study was performed on 2453 Italian patients followed prospectively from 28 dialysis centres over a 2-year period. Data were collected every 6 months and end points included time-to-death cumulative probability in patients with serum intact PTH (iPTH) ≤150 pg/mL and the effect of vitamin D receptor activation (VDRA) therapy. KaplanMeier curves and proportional hazards regression models stratified by PTH levels (i.e. ≤150 and >150 pg/mL) were used to determine cumulative probability of time-to-death and adjusted hazard ratios (HRs) for demographic, clinical and CKD-MBD treatment characteristics. Results. The cumulative probability of death was higher (P < 0.01) for patients with serum iPTH levels ≤150 pg/mL [25.1%, 95% confidence interval (CI): 22.128.5 at 18 months] versus those with serum iPTH levels within the normal range (18.0%, 95% CI: 16.120.1). In a model with time-dependent covariates restricted to time periods when patients had iPTH levels ≤150 pg/mL, lower mortality was observed in patients treated with VDRA [i.e. HR 0.62, 95% CI: 0.420.92 for oral or intravenous (IV) calcitriol; HR 0.18, 95% CI: 0.040.8 for IV paricalcitol] versus those not receiving any VDRA (P < 0.01) independently of other variables. Patients who received IV paricalcitol, compared with either oral or IV calcitriol, showed reduced mortality, but this was not statistically significant (HR = 0.3, 95% CI: 0.071.31, P = 0.11). Conclusion. Results from this observational study suggest that VDRA therapy was associated with improved survival in dialysis patients, even with low serum iPTH levels. © 2012 The Author. Source


Chiavarino C.,Polytechnic University of Turin | Chiavarino C.,Salesian Pontifical University | Bianchino C.,Polytechnic University of Turin | Brach-Prever S.,S. Giovanni Bosco Hospital | And 4 more authors.
Journal of Health Psychology | Year: 2015

This article provides the first assessment of theory of mind, that is, the ability to reason about mental states, in adult patients with congenital heart disease. Patients with congenital heart disease and matched healthy controls were administered classical theory of mind tasks and a semi-structured interview which provides a multidimensional evaluation of theory of mind (Theory of Mind Assessment Scale). The patients with congenital heart disease performed worse than the controls on the Theory of Mind Assessment Scale, whereas they did as well as the control group on the classical theory-of-mind tasks. These findings provide the first evidence that adults with congenital heart disease may display specific impairments in theory of mind. © 2015 SAGE Publications. Source


Vergano M.,S. Giovanni Bosco Hospital | Gristina G.R.,Study Group on Bioethics
Trends in Anaesthesia and Critical Care | Year: 2014

Futility represents a concept often used to justify withholding/withdrawing therapies and, at the same time, a shift in the physician's ethical obligations to patients. In this sense, one might expect that physicians would use clear criteria for determining when a therapy is futile. This is not true. Rather than being a discrete and definable entity, a therapy may be defined as futile merely when we cross the threshold of the therapies with very low efficacy. Decisions to withhold/withdraw therapy deemed as futile must follow both clinical evidence about the chance of success of a therapy and an explicit consideration of the patient's goals for therapy expressed by the patient when possible or their surrogates. © 2014 Elsevier Ltd. Source

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