Analisi e progettazione di un sistema di misure quantitative per il monitoraggio dei rischi finanziari delle garanzie di origine.

Lo scopo che si prefigge questo lavoro \ue8 quello di analizzare il mercato emergente delle Garanzie d\u2019Origine (GO), con particolare riferimento alla gestione dei rischi ad esse associati. Malgrado negli ultimi anni i volumi scambiati di queste certificazioni elettroniche abbiano segnato un incremento significativo, i mercati ad esse associati continuano ad essere poco trasparenti ed incompleti, per cui le informazioni e i dati a disposizione risultano essere molto limitati. A questo proposito, in letteratura non esiste quasi nessuno studio di riferimento, n\ue9 tantomeno una specifica normativa per la valutazione del rischio associato a tali strumenti. Questo lavoro suggerisce un possibile approccio alla gestione dei rischi associati alle GO che pu\uf2 costituire un utile riferimento per gli operatori che negoziano tali strumenti. A tal fine saranno presentate diverse tecniche di stima dei rischi di mercato, di liquidit\ue0 e di controparte che non devono essere considerate tra loro alternative, ma parti integranti di un approccio pi\uf9 generale. Poich\ue9 le serie storiche a disposizione sono brevi e caratterizzate da prezzi costanti per lunghi intervalli temporali, si intende proporre metodologie quantitative volte a valutare e gestire, in modo prudenziale, i principali rischi non sempre trattabili con approcci convenzionali

Adipose stem cell niche reprograms the colorectal cancer stem cell metastatic machinery

Obesity is a strong risk factor for cancer progression, posing obesity-related cancer as one of the leading causes of death. Nevertheless, the molecular mechanisms that endow cancer cells with metastatic properties in patients affected by obesity remain unexplored. Here, we show that IL-6 and HGF, secreted by tumor neighboring visceral adipose stromal cells (V-ASCs), expand the metastatic colorectal (CR) cancer cell compartment (CD44v6 +), which in turn secretes neurotrophins such as NGF and NT-3, and recruits adipose stem cells within tumor mass. Visceral adipose-derived factors promote vasculogenesis and the onset of metastatic dissemination by activation of STAT3, which inhibits miR-200a and enhances ZEB2 expression, effectively reprogramming CRC cells into a highly metastatic phenotype. Notably, obesity-associated tumor microenvironment provokes a transition in the transcriptomic expression profile of cells derived from the epithelial consensus molecular subtype (CMS2) CRC patients towards a mesenchymal subtype (CMS4). STAT3 pathway inhibition reduces ZEB2 expression and abrogates the metastatic growth sustained by adipose-released proteins. Together, our data suggest that targeting adipose factors in colorectal cancer patients with obesity may represent a therapeutic strategy for preventing metastatic disease

Adipose stem cell niche reprograms the colorectal cancer stem cell metastatic machinery

Obesity is a strong risk factor for cancer progression, posing obesity-related cancer as one of the leading causes of death. Nevertheless, the molecular mechanisms that endow cancer cells with metastatic properties in patients affected by obesity remain unexplored. Here, we show that IL-6 and HGF, secreted by tumor neighboring visceral adipose stromal cells (V-ASCs), expand the metastatic colorectal (CR) cancer cell compartment (CD44v6 + ), which in turn secretes neurotrophins such as NGF and NT-3, and recruits adipose stem cells within tumor mass. Visceral adipose-derived factors promote vasculogenesis and the onset of metastatic dissemination by activation of STAT3, which inhibits miR200a and enhances ZEB2 expression, effectively reprogramming CRC cells into a highly metastatic phenotype. Notably, obesity-associated tumor microenvironment provokes a transition in the transcriptomic expression profile of cells derived from the epithelial consensus molecular subtype (CMS2) CRC patients towards a mesenchymal subtype (CMS4). STAT3 pathway inhibition reduces ZEB2 expression and abrogates the metastatic growth sustained by adipose-released proteins. Together, our data suggest that targeting adipose factors in colorectal cancer patients with obesity may represent a therapeutic strategy for preventing metastatic diseas