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Our model predicts that the strength of selection for driver mutations determines whether a cancer is likely to evolve a mutator phenotype: in situations where selection for driver mutations is very weak, or very strong, a mutator phenotype is unlikely to evolve.
In lung cancer, the average number of mutations is very high with more than 8.9 mutations/Mb (Network TCGAR, 2014) that is to say more than 10,000 mutations/genome.
Because disease presentation in these patients with null mutations is very variable, ranging from mild to severe, we conclude that β-mannosidosis in humans may indeed be milder than typical of other lysosomal storage disorders.
The frequency of KRAS mutations is very high (~80%) in advanced pancreatic cancers [ 7, 63].
On the contrary, in cervical cancer the frequency of the p53 mutations is very low.
The wide phenotypic expression associated with PCDH19 mutations is very reminiscent of what is observed for patients with SCN1A mutations.
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This finding is important because p53 mutations are very common in STS, and p53-mutated STS are more therapeutically resistant [91].
Omitting tRNA modifications had little affect, but anticodon mutations were very inhibitory.
Some of these mutations are very common in certain areas, including parts of Asia and Africa.
These mutations are very useful for classical genetic studies as well as for modern techniques including functional genomics.
That the same genes are at work in many breeds indicates that these mutations are very old.
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Since I tried Ludwig back in 2017, I have been constantly using it in both editing and translation. Ever since, I suggest it to my translators at ProSciEditing.

Justyna Jupowicz-Kozak
CEO of Professional Science Editing for Scientists @ prosciediting.com