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Given that BRAF is more commonly mutated in melanomas, we hypothesized that targeting the BRAF effector arm alone would be sufficient to affect cell proliferation and in vivo tumor growth.
A similar enrichment was identified in genes involved in histone modification (EED, EZH2 and SUZ12), which were more commonly mutated in ETP ALL (42%) compared with non-ETP ALL (12% P=0.0001).
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One such example is multiplexed tumor genotyping (ie, panel testing) of more than 2800 mutations across 50 commonly mutated cancer-associated genes.
In solid tumors, P53 is commonly mutated and somatic mutations of P53 occur in more than 50% of human malignancies (Kruiswijk et al., 2015).
The gene encoding tumor suppressor p53 is commonly mutated in cancers, and contrary to the EGFR mutation, p53 mutations occur more frequently in smokers than in non-smokers (Ryberg et al., 1994; Garinis et al., 2001; Pfeifer et al., 2002).
The mutational status of sixty-four comutatedmutated cancer genes was assessed.
Twenty-nine genes were found to be mutated in more than 10% of patients (Fig. 1), including many commonly mutated genes in SCLC12.
We notice that TP53 is the most commonly mutated gene and is present in more than 80% of the high-grade serous ovarian carcinomas while all other genes are mutated in less than 27% of samples.
Regarding the mutations found, USH2A represents the most commonly mutated gene within our cohort of patients, with eleven different mutations found in this gene in seven patients characterized.
These two codons are the most commonly mutated ones in the entire p53 mutation database, and this is true in almost every type of human tumor.
The IDH1 gene was also among the most commonly mutated epigenetic genes within our collection and was more frequently mutated than reported in prior studies [ 20].
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