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A tumour starts as a single cell, which acquires mutations and eventually divides uncontrollably.
First, one of the copies can be silenced by the accumulation of deleterious mutations and eventually become indistinguishable from genomic non-coding neighboring regions, while the other copy retains the original function.
Persistent hyperproliferation could lead to increased accumulation of spontaneous mutations and eventually cancer.
Mice with conditional knockout of Dicer1 or Sbds in BM stromal cells developed dysplastic changes in hematopoietic cells, subsequent genetic mutations, and eventually leukemic transformation.
Although some copies may accumulate deleterious mutations and eventually cease to be functional (becoming pseudogenes), others may acquire, by chance, beneficial mutations and evolve under positive selection.
Stimulation of proliferation predisposes epithelial cells to occurrence of somatic mutations and eventually to malignant changes [ 5], especially during long-term HT [ 6, 7].
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It is well known that gene duplication, including retrotransposition, provides the opportunity for the duplicated genes to diverge by mutation and eventually change or acquire new functions.
If not detoxified these substances are capable of oxidizing membrane components and proteins and can lead to the degradation of nucleic acids, lipids, pigments, membranes, proteins, RNA, and DNA, causing mutation and eventually cell death [ 9- 11].
This observation is consistent with an evolutionary scenario wherein ORFan genes emerged and underwent a large number of random mutations and selection, eventually adapting to the composition preference of their organism over time.
This analysis suggests that genes that are not under strong selective pressure (evolve faster than others) in Salmonella tend to accumulate more AT-rich mutations and are eventually silenced by H-NS.
In order to develop a comprehensive approach for the detection of mutations and to eventually identify other genes responsible for resistance to anti-EGFR moAbs, we investigated a panel of 21 genes by parallel sequencing on the Ion Torrent Personal Genome Machine platform.
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Justyna Jupowicz-Kozak
CEO of Professional Science Editing for Scientists @ prosciediting.com