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EGFR or its signal transducers are mutated in 26.5% of cases: 4 samples bear mutations of PI3K (8.2%), 3 cases (6.1%) in K-RAS, 4 (8.2%) in B-RAF, and 2 cases (4.1%) in PTEN, but no loss of PTEN expression is detected.
Cancer cells bear mutations that enable rapid growth, but what if only some cells within a tumor possess indefinite growth?
This led us to speculate that GBMs might bear mutations in other regions of the AKT1 gene.
This p-value was used to sort the human genes by their propensity to bear mutations in cancer.
Moreover, we have observed that structurally conserved hotspots of cancer driver mutations often bear mutations with a high oncogenic activity (Figure 6B).
The absence of IDH1 and IDH2 mutations in our PXA cohort suggests that these mutations are rare or not present in PXA, a feature that can help discriminate PXA from the 87.5% of diffuse glioma that bear mutations in these gene [49].
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The next most common position mutated in FIPV is P2; >30% of the FIPVs analyzed bore mutations at this position.
However, of the four mutants selected with AS I Mabs, two bore mutations within AS I as expected while the remaining two carried mutations in AS II.
Taken together, we can conclude that all strains analyzed retained the relBE2Spn module, but exhibited three different genetic arrangements: 21.5%, 61.3% and 17.2% of the analyzed strains exhibited a genetic organization of the type I, II and III, respectively; 36% of the sequenced strains bore mutations in the gene encoding the RelE2Spn toxin.
Sixty-four tumors bore PIK3CA mutations located in exon 9, 86 tumors bore mutations in exon 20, and one tumor bore mutations in both exons 9 and 20 (Table 1).
First, neither strain bore mutations in known structural RNAs (also see point 1 below), so we lacked obvious candidates for buffering.
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