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Although in contrast to K14MycER mice, p53 is often mutated in sebaceous carcinoma (Kiyosaki et al., 2010) as a result of DNA damage, and these mutations are still capable of inhibiting AR activity when tested in prostate cells (Nesslinger et al., 2003).
The causes of mutations are still poorly understood.
The relevant mutations are still scattered among different strains.
Tests to detect cancer-causing mutations are still in their infancy.
Nevertheless, off-target mutations are still observed, and an additional gRNA could introduce new potential sites of off-target mutations.
This classification is not always easy to use, as some patients cannot be included (and some genetic mutations are still to be discovered), and it is usually more convenient in practice to distinguish between cases diagnosed before or at birth (i.e., severe forms of OI) and cases diagnosed after birth (i.e., milder forms of OI).
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Our ability to predict the thermodynamic consequences of even single point mutations is still surprisingly limited, and established methods of measuring stability are slow.
In this dataset, BRAF, KRAS, and NRAS mutations were still sensitive to MEK1/2 inhibitors (Fig. 3a, b).
If fecundity costs are present (i.e. f>0), then effective transmission rates remain below 1 so that subsequent spread of male-specific repressive mutations is still possible.
We thus conclude that the frequency of mutations is still within the normal range when NBS patients are compared to controls with a similar age.
However, the nature of inflammation-induced microsatellite mutations is still obscure.
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Justyna Jupowicz-Kozak
CEO of Professional Science Editing for Scientists @ prosciediting.com