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Our results support the hypothesis that oncogenic mutations can exert similar effects in diverse organs.
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Whilst many of the above diseases are characterized by mutations in protein coding regions, mutations can also exert deleterious effects through RNA molecules.
ALS-associated mutations can potentially exert a deleterious effect via two mechanisms loss of nuclear function and gain of toxic function in the cytoplasm.
By mimicking a genetic mutation, chemicals and drugs can exert both negative and positive effects on an existent mutation.
After exposure, PAH can exert genotoxic effects, inducing mutations, as well as epigenetic effects (Perera et al. 2009).
Moreover, mutations in such genes that should affect all mitochondrially encoded gene products can exert respiratory chain complex specific defects.
Even short insertions and deletions (indels) can exert important effects on genomes by locally increasing the mutation rate, with multiple mechanisms proposed to account for this pattern.
Recent studies have shown that both stromal architecture and composition can exert an important influence on normal epithelial biology [ 11, 40], and somatic mutations can be identified in the stromal compartment of breast tumours independently of mutations in the neoplastic epithelium [ 13, 14].
It has been reported that Gls2 can exert its tumor suppressive function via reduction of oxidative stress-induced DNA damage and mutations [ 15].
Studies have shown that both stromal architecture and composition can exert an important influence on normal epithelial homeostasis [ 16, 17, 42], and somatic mutations can be identified in the stromal compartment of breast tumors independently of mutations in the neoplastic epithelium [ 43, 44].
Still, they can exert powerful political pull.
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