Pathological and clinical parameters of gliomas with varying extent of PDGFRA expression.

<p>PDGFRA expression among the glioma samples in GSE16011 and the Rembrandt data sets was analyzed independent of morphological diagnosis. The samples with the upmost 25% of PDGFRA expression (PDGFRA-high) were compared with the samples with the lowest 25% of PDGFRA expression (PDGFRA-low) and the samples with the 50% intermediate levels of PDGFRA expression (PDGFRA intermediate) regarding frequencies of IDH1 mutation, age at diagnosis and survival period. The data on IDH1 mutation, LOH at 1p and 19q, and EGFR amplification for GSE16011 data set were derived from the results of Gravendeel et al <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0061556#pone.0061556-Gravendeel1" target="_blank">[27]</a>. The data on LOH in regions of 1p36 (1p36.23 or 1p36.32 or 1p36.31) and 19q13 (19q13.32 or 19q13.41) as analyzed by Mariani <i>et al.</i><a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0061556#pone.0061556-Mariani1" target="_blank">[47]</a>, and EGFR amplification for the Rembrandt data set were derived from GISTIC2.0 analysis of the 50K <i>HindIII</i> SNP array data <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0061556#pone.0061556-Madhavan1" target="_blank">[28]</a>. The differences for <i>IDH1</i> mutation rate, LOH at 1p and 19q and EGFR amplification were analyzed using chi-square test. The median age at diagnosis and survival period between the PDGFRA subgroups were analyzed using Fisher's exact test, One-way Anova and log-rank tests, respectively.</p>*<p>: Comparison with the PDGFRA-high group.</p>**<p>: The number of patients with known survival data.