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Because these mutations are irreversible and heritable, it is possible to identify mutated cells (and any cells descended from them) by their lack of CCO.
Because these mutations are likely to confer a selective advantage to the virus in the presence of R, they are currently under study.
Because these mutations are gradually eliminated over time, this is reflected in a steady decline in rates.
Because these mutations are present from early in development, a developmental cause of these phenotypes cannot be excluded.
Because these mutations are less common (30 vs. 70 % LOH), the proportion of those affected in these families may be lower [ 3, 17].
In addition, because these mutations are immediate to the cutting site, they should effectively block chiRNA recognition, thereby protecting the template.
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Because these mutations were unique to isolates sequenced during this study, our results did not show a closer genetic relationship to isolates from 2001, 2000, or 1999.
We sought mutations in the EGFR gene in TNBCs, because EGFR mutations were found in a subset of Japanese non-small lung cancers, despite being very rare in Caucasians [ 23], and because these mutations were suggested to predict responses to gefitinib therapy [ 23, 24].
That's important because those mutations are commonly medically relevant.
Selection against these mutations is weak because under natural conditions, most individuals die for other, external reasons before aging manifests itself.
Fixation of these mutations is expected because they have a net advantage due to a high ratio of benefit to realized-cost.
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