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A joint study between the groups of Valeria Poli and Enzo Calautti demonstrates that a moderate but sustained increase of STAT3 activity enhances epidermal stem cell properties, delays differentiation and favors spontaneous immortalization of keratinocytes.


Skin tumorigenesis is enhanced by overexpression in keratinocytes of the constitutively active STAT3C mutant, which also induces robust, psoriasis-like epidermal hyperplasia. In this paper published in Experimental Dermatology, Valeria Orecchia, Gabriella Regis and colleagues demonstrated that STAT3C expression at physiological levels in knock-in mice leads to mild epidermal hyperplasia and attenuated expression of terminal differentiation markers. This correlates with enhanced proliferative and clonogenic potential, attenuated senescence and, strikingly, high frequency spontaneous immortalization. These results suggest that moderate levels of continuous STAT3 activation, which mimic chronic inflammatory conditions, may establish a pre-neoplastic state in part by promoting the escape of epidermal progenitor cells from differentiation and senescence checkpoints.

The Bioinformatics & Genomics group together with the System Biology Group, at  the Computer Science Dept., have recently published on Bioinformatics chimera, a tool for secondary analysis of fusion events.

eciidjic.jpgChimera is a Bioconductor package that organizes, annotates, analyses and validates fusions reported by different fusion detection tools; current implementation can deal with output from bellerophontes, chimeraScan, deFuse, fusionCatcher, FusionFinder, FusionHunter, FusionMap, mapSplice, Rsubread, tophat-fusion and STAR. The core of Chimera is a fusion data structure that can store fusion events detected with any of the aforementioned tools. Fusions are then easily manipulated with standard R functions or through the set of functionalities specifically developed in Chimera with the aim of supporting the user in managing fusions and discriminating false-positive results. Pubmed id:

A paper from the Immunogenetics group demonstrates that the extracellular form of the NAD biosynthetic enzyme nicotinamide phosphoribosyltransferase (NAMPT) is a critical element in the induction of an immunosuppressive and tumor-promoting microenvironment in chronic lymphocytic leukemia (CLL).


NAMPT is the rate-limiting enzyme in NAD biosynthesis. In the extracellular compartment it exhibits cytokine/adipokine-like properties. Extracellular NAMPT (eNAMPT) levels are increased in various metabolic and inflammatory diseases as well as in tumors, rendering this pleiotropic molecule a novel player in tumor/host cross-talk. In this paper published in Blood /pubmed/25368373, Valentina Audrito and colleagues from the Immunogenetics Unit show that NAMPT levels are increased in CLL lymphocytes and that eNAMPT production is induced upon activation of the leukemic cells. In the CLL microenvironment, eNAMPT is an important element in inducing monocyte polarization to M2 macrophages secreting immunosuppressive and tumor promoting cytokines and reducing T cell responses. These effects are independent of the enzymatic activity of NAMPT, as inferred from the use of an enzymatically inactive mutant. Overall, these results reveal that eNAMPT is a critical element in the induction of an immunosuppressive and tumor-promoting microenvironment of CLL.

Ultimo aggiornamento: 25/02/2015 11:15
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