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In addition, genes, where methylation occurs in only one allele in combination with mutation or deletion of the other, show no HsK27me3 in normal cells suggesting that although HsK27me3 targets a subset of genes for methylation in cancer, methylation can also be driven by clonal natural selection in genes without pre-existent HsK27me3.
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These data further suggest that clonal architecture might be driven by genetic heterogeneity of propagating or 'stem' cells.
Clonal expansion is traditionally thought to be driven by genetic and epigenetic changes inherited by cell division [ 30].
Clonal expansion was initially hypothesized to be driven by a selective advantage for deleted mtDNA species over wild-type mtDNA molecules based upon replicative turnover (9).
Aging-associated increases in stem and progenitor cell mutations can in principle be driven by increases in mutation initiation rates and/or in the selection and clonal dominance of stem and progenitor cells that have acquired non-neutral mutations.
Be driven by the future.
The low diversity and the prevalence of a dominant sequence during the peak epidemic indicated that the peak epidemic was driven by a clonal expansion of very closely related sequences.
It is generally accepted that initiation and progression of cancers are driven by a process of clonal evolution.
This was driven by (1) expansion of pre-established clonal forest herbs and (2) invasion of graminoids and long-distance dispersers.
We further show that this surprisingly extensive variation in gene content within clonal species is driven by gene loss.
A simplistic model of clonal evolution is portrayed as a succession of clonal expansions, where each round is driven by the acquisition of additional random mutations [ 2, 13] that can be deleterious, neutral or confer a biological advantage (that is, proliferation and survival).
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