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Until now, Dr. Wilson said, most work on cancer mutations has focused on just a few hundred genes already suspected of being involved in the disease, not the 20,000 or so genes that make up the full human genome.
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Biochemical analyses of these mutations have focused on the kinase activity of LRRK2.
Most mechanistic studies dealing with GIST mutations have focused on c-KIT and far less is known about the signalling characteristics of the mutated PDGFRα proteins.
Most studies on mtDNA mutation have focused on sequencing of the D-loop region.
Most previous studies of mutation rate variation have focused on mammals.
Quasispecies theory treats multiple loci, whereas early work on mutation-selection balance has focused on one- or two-locus models.
By design, our analysis has focused on mutations with very large fitness effects.
Because of the low frequency of finding such complementary mutations, work on understanding transvection has focused on test cases including, but not limited to, the yellow (Geyer et al. 1990), Ultrabithorax (Lewis 1954), and white loci (Jack and Judd 1979; Gelbart and Wu 1982).
Based on the adenoma carcinoma sequence, much research has focused on mutation detection; sequential genetic alterations have been illustrated as a linear process (Fearon and Vogelstein, 1990; Kinzler and Vogelstein, 1996).
Extensive study has focused on initial mutations in carcinogenesis and led to seminal insights into the roles of oncogenes in tumor progression.
In contrast, determination of tumorigenic mechanisms has focused on somatic mutations.
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