We were unable to test whether differentially retained introns in IDH1 or IDH2-mutant samples exhibited differential DNA methylation due to the low probe coverage of introns on the Illumina HumanMethylation450K BeadChip used by TCGA.
Likewise, a groundbreaking study by Sturm and colleagues revealed distinct epigenetic subtypes of GBM, with K27 and G34 mutant tumor samples exhibiting independent gene expression and methylation profiles (Bjerke et al., 2013; Schwartzentruber et al., 2012; Sturm et al., 2012).
However, analysis of specific gene promoters shows mixed results in TET2 mutant samples, frequently exhibiting promoter-specific hypermethylation in spite of global hypomethylation (Perez et al., 2012; Wu et al., 2011; Yamazaki et al., 2012).
No samples exhibited inhibition.
Eleven samples exhibited titers >100.
However, we cannot rule out the possibility of dilution of mutant allele by the wild type allele in samples exhibiting p53 staining in less than 50% cells.
Wt strains containing plasmids typically exhibit 80 90% of white/sectored colonies and samples exhibiting <2% of integrations (i.e., white colonies in the mutants) were included in the quantification.
Using a p-value threshold of <10-5 to define statistically significant expression differences between hdac1 mutant and wild-type sibling samples, we observed that 4345 probes exhibited increased expression in the 27 hpf hdac1 <span class="lh">mutant samples, whereas 4142 probes exhibited decreased expression in these samples.
We also show that these tumor samples exhibit high expression of p53 compared with their adjacent normal tissues, indicating that these tumors may harbor mutant p53.
The CFUs of the wild-type strain showed highest infection in all four samples, whereas the ssn8 mutant exhibited the lowest cell counts in the brain, liver and cerebrospinal fluid (Fig. 9B).
