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Among these changes, there were both well-characterized mutations and mutations affecting aminoacid not previously found to be mutated in human cancers.
While p53 is mutated in human cancers, most human melanomas maintain wild-type conformation.
The gene that encodes the α-isoform of phosphatidylinositol 3-kinase (PIK3Ca) is frequently mutated in human cancers.
The mTOR/PI3K/AKT pathway is frequently mutated in human cancers and is thus an important oncology target.
RhoB, one of the upstream signaling proteins of the phosphatidylinositol-3-kinase (PI3K /Akt pathway, is frequently mutated in human cancer.
Multiple residues corresponding to the fumarate-binding site were mutated in human c-NADP-ME to correspond to those found in human m-NAD(P -ME.
Voltage-gated sodium (Nav) channels initiate and propagate action potentials in excitable cells, and are frequently dysregulated or mutated in human disease.
Although recent cancer genomics studies have identified a large number of genes that were mutated in human cancers, p53 remains as the most frequently mutated gene.
Two of the MMR proteins are most commonly mutated in human cancers, MLH1 and MSH2.
Multiple components of this pathway such as H, N, K-RAS and BRAF are often mutated in human cancer [1].
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Furthermore, optimal oncogene validation may require contextual modeling within a background of known and associated drivers that are co-mutated in human cancer.
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