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The present study revealed that PIK3CA mutations were more common in MSI and BRAF mutated tumours.
CALR mutations were more frequent in pre-PMF than in ET (35.8% vs 17.8%, P < 0.001).
We found that patient MHC-I genotype-based scores could predict which mutations were more likely to emerge in their tumor.
Our study demonstrates that low-frequency primary RAL-resistant mutations were uncommon, while minority secondary RAL-resistant mutations were more frequently detected in patients naïve to raltegravir.
Even though TP53 mutations were more frequent among younger patients with glioblastoma, they had no statistically significant effect on survival after adjustment for age (P = 0.62).
In our analysis, cells with BRAF mutations were more sensitive to BRAF inhibitors than cells with KRAS, NRAS, or EGFR mutations (Fig. 2b).
Interestingly, PTEN mutations were more common in the combined basal-like cell lines (P = 0.020), while PIK3CA mutations were more frequent in luminal lines (P = 0.022).
EGFR mutations were more frequently observed in never-smokers (P = 0.03) and females (P = 0.0001).
In patients younger than 50 years (n = 45), PIK3CA mutations were not observed and TP53 mutations were more frequent than in the older age groups.
Mutations were more prevalent in SM than MM (81% vs. 58%, OR 3.18 [0.6;18.3]) and also showed an higher rate of triple mutations (46% versus 31% of SM and MM respectively, OR NS).
Thymidine associated mutations were more frequent in multiexperienced patients.
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