The rate of the G1613A and C1653T mutations were significantly higher in patients with HCC (Table 4).
Interestingly, spliceosome mutations were significantly less represented in CALR-mutated patients; however, no additional molecular or cytogenetic correlate was highlighted.
Tumor genomes with TP53 mutations were significantly more unstable than those without TP53 mutations.
Furthermore, Hakimi and colleagues found that SETD2 mutations were significantly associated with worse cancer-specific survival (CSS) in ccRCC (Hakimi et al., 2013b).
Two additional cell lines, QG56 (expressing wtEGFR) and NCI-H1975 (expressing the L858R + T790M point mutations), were significantly less sensitive to erlotinib treatment, with mean IC50 values of 8.9 and 4.3 μM, respectively.
On the other hand, de novo mutations were significantly induced in stem cell spermatogonia (Figure 3, Table 1).
For each assay, the mean ΔCTs of the specimens documented to have mutations were significantly lower than the ΔCTs of the wildtype samples (all p values <0.0001, T-test).
TP53 mutations were significantly associated with CD vs PD (P=0.037; Table 3).
None of the other mutations were significantly correlated with LRFS or overall survival.
LR mutations were significantly more common in Latin American/Caribbean patients.
We found that IDH mutations were significantly associated with MGMT promoter methylation (P < 0.0001).
