@article {8300,
	title = {Iron signature in asbestos-induced malignant pleural mesothelioma: A population-based autopsy study.},
	journal = {J Toxicol Environ Health A},
	volume = {79},
	year = {2016},
	month = {2016},
	pages = {129-41},
	abstract = {<p>Malignant pleural mesothelioma (MPM) is an aggressive cancer with poor prognosis. The development of MPM is frequently linked to inhalation of asbestos fibers. A genetic component of susceptibility to this disease is suggested by the observation that some individuals develop MPM following lower doses of asbestos exposure, whereas others exposed to higher quantities do not seem to be affected. This hypothesis is supported also by frequent reports of MPM familial clustering. Despite the widely recognized role of iron (Fe) in cellular asbestos-induced pulmonary toxicity, the role of the related gene polymorphisms in the etiology of MPM has apparently not been evaluated. Eighty-six single-nucleotide polymorphisms (SNPs) of 10 Fe-metabolism genes were examined by exploiting formalin-fixed paraffin-embedded postmortem samples from 77 patients who died due to MPM (designated AEM) and compared with 48 who were exposed to asbestos but from died in old age of cause other than asbestos (designated AENM). All subjects showed objective signs of asbestos exposure. Three SNPs, localized in the ferritin heavy polypeptide, transferrin, and hephaestin genes, whose frequencies were distributed differently in AEM and AENM populations, were identified. For ferritin and transferrin the C/C and the G/G genotypes, respectively, representing intronic polymorphisms, were significantly associated with protection against MPM and need to be considered as possible genetic markers of protection. Similarly, the C/C hephaestin SNP, a missense variation of this multicopper ferroxidase encoding gene, may be related, also functionally, with protection against MPM. In conclusion, it is proposed that three Fe metabolism-associated genes, significantly associated with protection against development of MPM, may serve as protective markers for this aggressive tumor.</p>},
	keywords = {Adult, Aged, Asbestos, Autopsy, Case-Control Studies, Female, Ferritins, Gene Frequency, Genetic Markers, Humans, Iron, Lung Neoplasms, Male, Membrane Proteins, Mesothelioma, Middle Aged, Mutation, Missense, Polymorphism, Single Nucleotide, Transferrin, Young Adult},
	issn = {1528-7394},
	doi = {10.1080/15287394.2015.1123452},
	author = {Crovella, Sergio and Bianco, Anna Monica and Vuch, Joseph and Zupin, Luisa and Moura, Ronald Rodrigues and Trevisan, Elisa and Schneider, Manuela and Brollo, Alessandro and Nicastro, Enza Maria and Cosenzi, Alessandro and Zabucchi, Giuliano and Borelli, Violetta}
}
@article {1844,
	title = {Inflammation profile of four early onset Crohn patients.},
	journal = {Gene},
	volume = {493},
	year = {2012},
	month = {2012 Feb 10},
	pages = {282-5},
	abstract = {<p>Crohn disease (CD) is a multifactorial disorder affecting mainly young adults. Sometimes, however, it can present in the first year of life (Early onset Crohn disease (EOCD)) showing an unpredictable course and can often be more severe than at older ages. Some cases have been associated to an underlying primary immunodeficiency such as IL10R deficiency. We studied the functional response to IL-10 and the genotype of IL-10 receptor in four patients with early onset crohn-like colitis. We found an IL10R variant, which may be associated with a decreased response to the cytokine in one patient. Further studies to determine its pathogenic effect should be performed. In addition IL-10 mediated inhibition of LPS-induced TNFα expression was measured in patient{\textquoteright}s monocytes.</p>},
	keywords = {Crohn Disease, Cytokines, Humans, Inflammation, Monocytes, Nod2 Signaling Adaptor Protein, Polymorphism, Genetic, Receptors, Interleukin-10, Tumor Necrosis Factor-alpha},
	issn = {1879-0038},
	doi = {10.1016/j.gene.2011.11.043},
	author = {Marcuzzi, Annalisa and Girardelli, Martina and Bianco, Anna Monica and Martelossi, Stefano and Magnolato, Andrea and Tommasini, Alberto and Crovella, Sergio}
}
