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A mechanism that was confirmed in human squamous cell lung carcinomas, where those cases harboring p53 mutations presented very high levels of VRK1 protein [33].
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The mutation logic was very simple.
However, this phenomenon presented very diversified situations.
It is known that HIV-1 can present very high mutation and recombination rates, however the specific contribution of these evolutionary forces in the "in vitro" viral fitness recovery has not been simultaneously quantified.
And while Dr Scott Hebbring, from the University of Wisconsin, described the study as "fascinating" he also cautioned that diseases can present very differently even between patients that have same mutations.
Mutations in NPHS2 are a common cause of SRNS and usually present very early in life [ 1, 3].
These low level "false" variants cause difficulty in identifying real somatic mutations present at very low fraction (e.g. less than 2%%) in the sample.
Having very high sequencing coverage is especially important for discovering cancer mutations present at low fractions.
Interestingly, although the IVS6-2A>G mutation, presented here, and the IVS4-2A>G mutation [11] are located very closely to each other, it is unclear why these patients differ in clinical phenotype.
It is also reported that cancer cells having HER2 mutations, present in a very small fraction of NSCLC, are insensitive to EGFR-TKI, but remain sensitive to HER2-targeted therapies (Wang et al, 2006).
He presents himself very, very well.
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Justyna Jupowicz-Kozak
CEO of Professional Science Editing for Scientists @ prosciediting.com