@article{EnjuanesFernandezHernandezetal.2011,
  author    = {Enjuanes, Anna and Fernandez, Veronica and Hernandez, Luis and Navarro, Alba and Bea, Silvia and Pinyol, Magda and Lopez-Guillermo, Armando and Rosenwald, Andreas and Ott, German and Campo, Elias and Jares, Pedro},
  title     = {Identification of Methylated Genes Associated with Aggressive Clinicopathological Features in Mantle Cell Lymphoma},
  series = {PLoS ONE},
  volume    = {6},
  journal   = {PLoS ONE},
  number    = {5},
  doi       = {10.1371/journal.pone.0019736},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-140632},
  pages     = {e19736},
  year      = {2011},
  abstract  = {Background: Mantle cell lymphoma (MCL) is genetically characterized by the t(11; 14)(q13; q32) translocation and a high number of secondary chromosomal alterations. The contribution of DNA methylation to MCL lymphomagenesis is not well known. We sought to identify epigenetically silenced genes in these tumours that might have clinical relevance. Methodology/Principal Findings: To identify potential methylated genes in MCL we initially investigated seven MCL cell lines treated with epigenetic drugs and gene expression microarray profiling. The methylation status of selected candidate genes was validated by a quantitative assay and subsequently analyzed in a series of primary MCL (n = 38). After pharmacological reversion we identified 252 potentially methylated genes. The methylation analysis of a subset of these genes (n = 25) in the MCL cell lines and normal B lymphocytes confirmed that 80\% of them were methylated in the cell lines but not in normal lymphocytes. The subsequent analysis in primary MCL identified five genes (SOX9, HOXA9, AHR, NR2F2, and ROBO1) frequently methylated in these tumours. The gene methylation events tended to occur in the same primary neoplasms and correlated with higher proliferation, increased number of chromosomal abnormalities, and shorter survival of the patients. Conclusions: We have identified a set of genes whose methylation degree and gene expression levels correlate with aggressive clinicopathological features of MCL. Our findings also suggest that a subset of MCL might show a CpG island methylator phenotype (CIMP) that may influence the behaviour of the tumours.},
  language  = {en}
}
@article{SchmittKellerNourkamiTutdibietal.2011,
  author    = {Schmitt, Jana and Keller, Andreas and Nourkami-Tutdibi, Nasenien and Heisel, Sabrina and Habel, Nunja and Leidinger, Petra and Ludwig, Nicole and Gessler, Manfred and Graf, Norbert and Berthold, Frank and Lenhof, Hans-Peter and Meese, Eckart},
  title     = {Autoantibody Signature Differentiates Wilms Tumor Patients from Neuroblastoma Patients},
  series = {PLoS ONE},
  volume    = {6},
  journal   = {PLoS ONE},
  number    = {12},
  doi       = {10.1371/journal.pone.0028951},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-133794},
  pages     = {e28951},
  year      = {2011},
  abstract  = {Several studies report autoantibody signatures in cancer. The majority of these studies analyzed adult tumors and compared the seroreactivity pattern of tumor patients with the pattern in healthy controls. Here, we compared the autoimmune response in patients with neuroblastoma and patients with Wilms tumor representing two different childhood tumors. We were able to differentiate untreated neuroblastoma patients from untreated Wilms tumor patients with an accuracy of 86.8\%, a sensitivity of 87.0\% and a specificity of 86.7\%. The separation of treated neuroblastoma patients from treated Wilms tumor patients' yielded comparable results with an accuracy of 83.8\%. We furthermore identified the antigens that contribute most to the differentiation between both tumor types. The analysis of these antigens revealed that neuroblastoma was considerably more immunogenic than Wilms tumor. The reported antigens have not been found to be relevant for comparative analyses between other tumors and controls. In summary, neuroblastoma appears as a highly immunogenic tumor as demonstrated by the extended number of antigens that separate this tumor from Wilms tumor.},
  language  = {en}
}