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These once-mutated cells can, with a certain probability, acquire the second mutation, which makes them fully malignant.
Both conditions are caused by a single DNA mutation, which makes them relatively easy to detect.
In addition, it contains a D76A mutation, which makes the inhibitory propeptide resistant to proteolysis [3].
In other words, even though the T315I mutation does not confer resistance to K, there may be a different mutation which makes the cell resistant to both K and I, but not to D. In this situation, treating with I and K is obviously better than just treating with I (this follows from our previous results), but what is interesting, adding D does give an advantage in this case.
There are genetic tests that help determine if a woman has inherited the gene mutation which makes one susceptible to ovarian cancer.
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In these circumstances a mutation which made it easier for big brains to evolve might do well.
It is of interest to note that in the mutagenesis study (Figure 4), the critical "C" mutation occurred at the 3' end of the shRNA, outside the "seed region," and the "T" mutation, which made MTp even less active than 3p, occurred outside the canonical 22-mer sequence of a mature miRNA.
However, it is limited by labeling efficiency, technical complexity, and crucially, the risk of incorporating random mutations which makes them unsuitable in the clinic.
Pseudo-gene has some deleterious mutations, which makes it non-functional.
Their shoots, runners, branches or subcolonies (=ramets sensu Jackson et al. 1985)) allow for a replication of identical genetic material (barring somatic mutations), which makes a comparison of tolerances and associated reaction norms straightforward.
We introduce an operation we call "global parallel mutate," which makes identical mutations in any number of populations.
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