@article {8328,
	title = {In vitro sensitivity to methyl-prednisolone is associated with clinical response in pediatric idiopathic nephrotic syndrome.},
	journal = {Clin Pharmacol Ther},
	volume = {100},
	year = {2016},
	month = {2016 Sep},
	pages = {268-74},
	abstract = {<p>The aim of this study was to evaluate the in vitro steroid sensitivity as a predictor of clinical response to glucocorticoids in childhood idiopathic nephrotic syndrome (INS). Seventy-four patients (median age 4.33, interquartile range [IQR] 2.82-7.23; 63.5\% male) were enrolled in a prospective multicenter study: in vitro steroid inhibition of patients{\textquoteright} peripheral blood mononuclear cell proliferation was evaluated by [methyl-(3) H] thymidine incorporation assay at disease onset (T0) and after 4 weeks (T4) of treatment. Steroid dependence was associated with increased in vitro sensitivity at T4 assessed both as drug concentration inducing 50\% of inhibition (IC50 ; odds ratio [OR] = 0.48, 95\% confidence interval [CI] = 0.24-0.85; P = 0.0094) and maximum inhibition at the highest drug concentration (Imax ; OR = 1.13, 95\% CI = 1.02-1.31; P = 0.017). IC50 > 4.4 nM and Imax < 92\% at T4 were good predictors for optimal clinical response. These results suggest that this test may be useful for predicting the response to glucocorticoid therapy in pediatric INS.</p>},
	issn = {1532-6535},
	doi = {10.1002/cpt.372},
	author = {Cuzzoni, E and De Iudicibus, S and Stocco, G and Favretto, D and Pelin, M and Messina, G and Ghio, L and Monti, E and Pasini, A and Montini, G and Decorti, G}
}
@article {1890,
	title = {Letter: TPMT activity and age in IBD patients.},
	journal = {Aliment Pharmacol Ther},
	volume = {35},
	year = {2012},
	month = {2012 Apr},
	pages = {966-7; author reply 967-9},
	keywords = {Azathioprine, Humans, Immunosuppressive Agents, Inflammatory Bowel Diseases, Thioguanine},
	issn = {1365-2036},
	doi = {10.1111/j.1365-2036.2012.05027.x},
	author = {Stocco, G and De Iudicibus, S and Cuzzoni, E and Decorti, G and Martelossi, S and Ventura, A}
}
@article {1760,
	title = {A genome-wide approach identifies that the aspartate metabolism pathway contributes to asparaginase sensitivity.},
	journal = {Leukemia},
	volume = {25},
	year = {2011},
	month = {2011 Jan},
	pages = {66-74},
	abstract = {<p>Asparaginase is an important component for treatment of childhood acute lymphoblastic leukemia (ALL). The basis for interindividual differences in asparaginase sensitivity remains unclear. To comprehensively identify genetic variants important in the cytotoxicity of asparaginase, we used a genome-wide association approach using the HapMap lymphoblastoid cell lines (87 CEU trio members) and 54 primary ALL leukemic blast samples at diagnosis. Asparaginase sensitivity was assessed as the drug concentration necessary to inhibit 50\% of growth (inhibitory concentration (IC)(50)). In CEU lines, we tested 2,390,203 single-nucleotide polymorphism (SNP) genotypes at the individual SNP (P<0.001) and gene level (P<0.05), and identified 329 SNPs representing 94 genes that were associated with asparaginase IC(50). The aspartate metabolism pathway was the most overrepresented among 199 pathways evaluated (P=8.1 {\texttimes} 10(-3)), with primary involvement of adenylosuccinate lyase and aspartyl-tRNA synthetase genes. We validated that SNPs in the aspartate metabolism pathway were also associated with asparaginase sensitivity in primary ALL leukemic blast samples (P=5.5 {\texttimes} 10(-5)). Our genome-wide interrogation of CEU cell lines and primary ALL blasts revealed that inherited genomic interindividual variation in a plausible candidate pathway can contribute to asparaginase sensitivity.</p>},
	keywords = {Antineoplastic Agents, Asparaginase, Aspartic Acid, Cell Line, Genome-Wide Association Study, Humans, Multivariate Analysis, Polymorphism, Single Nucleotide, Precursor Cell Lymphoblastic Leukemia-Lymphoma},
	issn = {1476-5551},
	doi = {10.1038/leu.2010.256},
	author = {Chen, S-H and Yang, W and Fan, Y and Stocco, G and Crews, K R and Yang, J J and Paugh, S W and Pui, C-H and Evans, W E and Relling, M V}
}
