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In an effort to identify potential molecular targets, limited mutational studies in primary or recurrent LGSC samples have revealed an overall low mutation frequency, with exome sequencing by Jones et al. showing an average of 10 validated somatic mutations (or 7.5 somatic non-synonymous or splice site mutations) per tumor [ 10].
HNPCC patients showed a significant increase in mutation frequency with age (Mann-Whitney U, P = 0.02).
Statistical analysis was performed to correlate the CDH1 mutation frequency with gastric cancer incidence areas.
Although there was a clear trend towards increasing mutation frequency with increasing age, substantial individual differences were also observed.
Integration of mutation frequency with TSG-OCG network provided insights that TSGs and OCGs might jointly contribute to the cancer development.
The mutation frequency with 30.0 keV μm-1 was approximately two-fold higher than that in the other irradiation conditions (Table 1).
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To compare our whole genome mutation frequencies with phenotype-selected mutation frequencies, we used a one-way frequency table with χ analysis.
The greater mutation frequencies with fixed versus fresh DNA extracted from the same tissue are consistent with translesion synthesis during PCR across sites of base damage.
We observed a highly significant correlation of mutation frequencies with the subject's age, a correlation that was stable in several of the markers and subject subgroups studied.
This selection should result in driver mutations occurring more frequently in tumor samples; hence, the most common approach for identifying driver mutations is based on calculating mutation frequencies with the assumption that a higher prevalence implies functionality.
It was expected that somatic mutation testing from such a large cohort of NSCLC patients would provide more reliable results for interpreting the association of mutation frequencies with patient demographics.
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