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TP53 mutation occurred more frequently in carcinomas than borderline tumors (56.8 % and 11.5 %, respectively), and combined IHC and mutation data suggest alterations occur in approximately 68 % of MC and as many as 20%% of MBOT.
Analysis of the compiled p53 mutation data suggest that, in addition to lifetime cumulative exposure to cigarette smoke, also stopping smoking for years prior to clinical manifestation of the disease may affect the incidence of p53 mutations.
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However, the rapid increase in cancer gene mutation data suggests a high level of complexity related to understanding the tumorigenic process [2].
All the mutated aa's were highly conserved across different mammalian species, and this combined with the lack of variation data suggest that these mutations are likely to be pathogenic.
The significant differences between these rhodopsin structures, the relatively low sequence homology between individual GPCRs, and some difficulties in rationalizing point-mutation data suggests that homology-based molecular modeling alone will not provide the accurate structural information on individual receptors required for ligand design and in silico screening.
Combined with the results of this study showing that patient-related truncated protein mutants are unstable and catalytically inactive and therefore loss of protein function mutations, these data suggest that PCTAIRE-1 plays an important role for normal brain development and function and hence its expression and activity need to be tightly regulated.
Although we do not have ancillary information on whether the genetic loci examined in this study have distinct mutation rates, our data suggest a model of neutral evolution for both loci (Table 3).
As opposed to the rare mutations, the present data suggest that common BCHE variations, particularly rs2668207 and rs2048493, are associated with subtle changes (4.3 9.5%) in cholinesterase activity across all four time points.
Evidence from patterns of shared mutations and polymorphism data suggest that multiple source genes are actively retrotransposing in the AluYh7 and AluYi6 subfamilies, the latter of which may contain up to 14 source elements.
There is insufficient information available to reach such a conclusion, although there are mutation data that suggest this is the case (Doak et al., 2007).
These data suggest mutation sets that abrogate binding to broadly neutralizing antibodies with greater specificity than the canonical mutation D368R, useful in rapidly assessing the nature of a vaccine response.
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