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Comparison to estimates of this quantity suggests that, as expected, recessive lethal mutations are only a subset of the recessive mutational burden.
In current clinical practice, gene mutations are only classified as being present or absent, ignoring the clonal complexity of cancers.
These mutations are only observed in a minority of patients and families, [9, 10] suggesting the presence of mutations in additional genes, which remain unknown at present.
Visible mutations are only part of the entire genetic variability, which includes polymorphisms.
While MEN1 mutations are only tumorigenic within neuroendocrine lineages, menin is expressed in most tissues, at all stages of development and likely has a universal function [7], [8].
Synthetic lethal interactions, where mutations are only lethal in combination, are generally considered to reflect such interactions within and between cascades, with parallel or compensatory pathways explaining most, though not all, synthetic lethal interactions [1], [7] [8].
Similar(26)
Tumor mutations were only found in one of them.
In contrast, the inhibitory effects of TGFbRII and ACTRIIA mutations were only observed in the cells stably expressing the receptor mutants, suggesting a possibly involvement of other unidentified mechanisms that require further investigation.
The codon 61 mutations were only found in samples from the >70 age group.
Some RTI (K65R, L74V) and PI (D30N, M46I/L, I84V) mutations were only seen in subtype B isolates.
Mutations were only found in the coding regions of the pyrF and pyrE2 genes and a number of mutants had mutations in more than one gene (Table 1).
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Justyna Jupowicz-Kozak
CEO of Professional Science Editing for Scientists @ prosciediting.com