@article {8329,
	title = {Differential expression of GAS5 in rapamycin-induced reversion of glucocorticoid resistance.},
	journal = {Clin Exp Pharmacol Physiol},
	volume = {43},
	year = {2016},
	month = {2016 Jun},
	pages = {602-5},
	abstract = {<p>This study evaluates the association between the long noncoding RNA GAS5 levels and the anti-proliferative effect of the glucocorticoid (GC) methylprednisolone (MP) alone and in combination with rapamycin in peripheral blood mononuclear cells (PBMCs) obtained from healthy donors. The effect of MP, rapamycin, and MP plus rapamycin was determined in 17 healthy donors by labelling metabolically active cells with [methyl-3H] thymidine and the expression levels of GAS5 gene were evaluated by real-time RT-PCR TaqMan analysis. We confirmed a role for GAS5 in modulating GC response: poor responders presented higher levels of GAS5 in comparison with good responders. Interestingly, when PBMCs were treated with the combination of rapamycin plus MP, the high levels of GAS5 observed for each drug in the MP poor responders group decreased in comparison with rapamycin (P value~=~0.0134) or MP alone (P value~=~0.0193). GAS5 is involved in GC resistance and co-treatment of rapamycin with GCs restores GC effectiveness in poor responders through the downregulation of the long noncoding RNA. GAS5 could be considered a biomarker to personalize therapy and a novel therapeutic target useful for the development of new pharmacological approaches to restore GC sensitivity.</p>},
	issn = {1440-1681},
	doi = {10.1111/1440-1681.12572},
	author = {Lucaf{\`o}, Marianna and Bravin, Vanessa and Tommasini, Alberto and Martelossi, Stefano and Rabach, Ingrid and Ventura, Alessandro and Decorti, Giuliana and De Iudicibus, Sara}
}
@article {1806,
	title = {Differential action of 3-hydroxyanthranilic acid on viability and activation of stimulated lymphocytes.},
	journal = {Int Immunopharmacol},
	volume = {11},
	year = {2011},
	month = {2011 Dec},
	pages = {2242-5},
	abstract = {<p>Lymphocytes proliferation after antigen-driven activation leads to an increase in cell count, which could last some week, until apoptosis mechanisms allow the homeostatic control of the system. During the first days of this stimulation, activated lymphocytes display high resistance to apoptosis and to most immunosuppressive drugs. According to the literature, few compounds have been described to kill recently activated cells, by inhibiting metabolic processes fundamental to proliferation. The aim of our work was to evaluate comparatively these different compounds, in order to identify the best strategy to kill cells that have undergone proliferation, while sparing the repertoire of resting cells. After preliminary experiments, 3-HAA and bortezomib were selected as the most suitable compounds for our purposes. The possible synergic effect of 3-HAA with bortezomib or with manganese ions was also assessed. 3-HAA was confirmed to be the most reliable pharmacologic approach to inhibit proliferation with acceptable toxicity on resting cells. While in the case of PHA stimulation 3-HAA led to death of most lymphocytes, only a minor percentage of cells were killed after allo-stimulation, suggesting that the effect is proportional to the percentage of stimulated lymphocytes. Manganese ions further enhanced this effect, while results with bortezomib seemed to be less consistent. These results deserve further investigations to develop new procedures for targeting activated cells with pharmacological approaches.</p>},
	keywords = {3-Hydroxyanthranilic Acid, Boronic Acids, Cell Survival, Cells, Cultured, Humans, Lymphocyte Activation, Lymphocytes, Manganese, Pyrazines},
	issn = {1878-1705},
	doi = {10.1016/j.intimp.2011.09.009},
	author = {Piscianz, Elisa and Cuzzoni, Eva and De Iudicibus, Sara and Valencic, Erica and Decorti, Giuliana and Tommasini, Alberto}
}
