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Exact(5)
The frequency of MED12 exon 2 mutations was analysed in altogether 1158 tumours by direct sequencing.
The presence of EGFR, KRAS, BRAF and PIK3CA mutations was analysed in 5125 lung cancer patients; 2072 of them were female (40.4%) and 3053 male (59.6%).
Presence of the BRAF V600E (a1796t) mutation, p53 mutation (over exons 4 8) and KRAS mutation (over codons 2 and 3) had been previously investigated for the RBWH's samples [ 17]; presence of BRAF V600E (a1796t) and KRAS (codons 2 and 3) mutations was analysed for Envoi's samples as previously described [ 17, 20- 22].
The presence of K- ras -2 mutations was analysed in tissue from 18 patients with VC associated HCCs.
By mistake, the full spectrum of to date known germline mutations was analysed, which is not cost effective.
Similar(55)
For mutational analysis, DNA was extracted from paraffin-embedded tissues and EGFR mutations were analysed by direct sequence of PCR products.
Samples (n = 39) of patients with either idiopathic erythrocytosis or PV from our previous report [11] which were negative by AS-PCR for exon 12 mutations were analysed by the HRM method and were again found negative.
The relative expression of each gene was characterized by the median and range, and the differences in gene expression between tumors with and without PIK3CA mutations were analysed for significance with the non parametric Mann-Whitney U test.
Synonymous and non-synonymous mutations were analysed on contig sequences.
KRAS mutations were analysed using archival tumour or plasma samples.
Therefore, the abundance of E-cadherin was determined and E-cadherin gene (CDH1) mutations were analysed.
Related(15)
variants was analysed
mutations was discussed
mutations was characterized
mutations was calculated
variations was analysed
mutations was ascertained
mutations was investigated
mutants was analysed
mutations was evaluated
mutations was explained
mutations was assessed
mutations was classified
mutations was explored
mutations was examined
mutations was quantified
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