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We predict that BRCA1 and BRCA2 mutations are approximately equal in our population.
Again, effectively neutral and advantageous mutations are approximately separated at s ≈ 1/ N e.
86 Frequencies of other gene mutations are approximately 10% or below 10%.
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These results provide some support for the use of Gumbel-type extreme value theory in studies of adaptation and point to a surprising connection between recent phenotypic- and sequence-based models of adaptation: in both, the distribution of fitness effects among rare beneficial mutations is approximately exponential.
The median length of these mutations was approximately 28 kb and the total average genome coverage was 4.2 Mb per cell line.
The prevalence of TNNI3 mutations is approximately 5% in HCM.
The prevalence of BRCA1 mutations was approximately twice the prevalence of BRCA2 mutations.
The overall incidence of TP53 mutations is approximately 30%40%% in tumor biopsies and approximately 60%70%% in established BL cell lines, regardless of the EBV status of the tumors.
The percentage of frameshift mutations was approximately 50% in most studies [ 21, 26], comparable to the 48% observed in the current study.
The frequency of KRAS exon 2 mutations is approximately 35 40% in colorectal cancer patients, and the frequency of other RAS mutations is 10 15%; the same trend exists in Europe and the USA, and Japan (Table 4).
As a protein evolves toward higher stability, the distribution of is constant but the selective pressure relaxes until the expected change in fitness, or alternatively the equilibrium average value of S for accepted mutations, is approximately zero.
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