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EGFR mutations were strong correlations between both EGFR mutation status in the tumour samples and serum samples and objective response to gefitinib (P<0.001).
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We observed that divergence among replicate populations was greater in environments with alternating resources than in environments with the same resources presented either singly or simultaneously, suggesting that epistatic interactions among mutations were stronger or more influential under the temporally fluctuating regimes.
Activating KRAS mutations are strong independent negative predictors of response to such treatment and mutational testing has been included in colorectal cancer practice guidelines.
In other words, if all mutations that a hybridogen carries affect fitness, regardless whether they reside on the sexually or clonally transmitted part of the genome, selection against all newly acquired mutations is strong if mutations interact synergistically, because of the "borrowed" high mutational load on the paternal genome.
Epidermal growth factor receptor (EGFR) mutations are strong determinants of tumor response to EGFR tyrosine kinase inhibitors in non-small cell lung cancers (NSCLCs).
Three sets of data demonstrated that glycolytic mutations are strong dnaE(Ts) suppressors.
All 23 mutations are strong suppressors of PEV, but none affected TPE.
Both garz mutations are strong loss of function/null alleles.
Being able to develop a mutator phenotype accelerated tumorigenesis (Fig. 4B), although the accelerating effect was reduced when selection for additional driver mutations was strong.
Epidermal growth factor receptor (EGFR) mutations are strong determinants of tumour response to EGFR tyrosine kinase inhibitors in non-small-cell lung cancer (NSCLC).
Assuming no CpG effect in CpG islands, these comparative results indicate that the influence of CpG→TpG/CpA mutations was strong in intergenic regions and even stronger in exons.
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CEO of Professional Science Editing for Scientists @ prosciediting.com