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This is in close agreement with the somatic mutation rate reported for PTPRS by DFCI (57/619, 9.2%)6 (Supplementary Fig. 3).
This low rate of true mutation, 7%, is similar to the mitochondrial HVI mutation rate reported using other methods [29].
No open reading frame is completely fixed at any locus, but this is expected due to the high slipped-strand mutation rate reported for these sites [9], [15].
Although the sample size is very small, the rate of change, two out of twenty-eight samples (7%), is consistent with the average mutation rate reported by others [28].
Again, one would expect probe choice to influence the mutation rate reported.
This is similar to the mutation rate reported in a study by Pal et al. [ 22] in young black African American breast cancer patients (9 %; 13/144).
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In ovarian cancer, mutations most often affect codons 12 and 13 of the KRAS gene, with mutation rates reported to be as high as 3 11% [ 3, 4].
The experimentally determined evolutionary models were constructed from the inferred amino-acid preferences reported here and the experimentally measured mutation rates reported in Bloom (2014).
This is much lower than would have been expected, based on the 35 40% KRAS mutation rates reported in primary tumours (Andreyev et al, 1998).
We assumed minimum and maximum values of a range of average mutation rates reported for synonymous sites of plant chloroplast genes [i.e., 1.2 and 1.7 × 10-9 substitutions per site per year (s/s/y)] for the BEAST analysis [ 55].
Therefore, the minimum and maximum values of a range of average mutation rates reported for synonymous sites of plant chloroplast genes [i.e. 1.2 and 1.7 × 10−9 substitutions per site per year (s/s/y)] were taken [ 26].
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