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It may be that clonal expansion of a cell(s) with a specific TP53 mutation is often a late event (i.e., dysplasia to carcinoma), while isolated aneuploid cells in earlier precursor cell populations sustain distinct TP53 mutations in a majority of those cells that progress toward cancer.
Destabilization of a structured protein domain by a mutation is often harmful [ 17].
Moreover, the assumption of weak selection and mutation is often overlooked in the literature, although, as we have demonstrated, it has profound implications for inferences.
The tumor harboring p53 mutation is often defective in transcription activity [ 53]; mice expressing defective p53 transcription activity are predisposed to tumors [ 4].
The tumor suppressor protein p53 is a transcription factor that functions as a cellular gatekeeper and its mutation is often associated with the development of cancers.
In an evolving asexual population, the actual rate of spread of a beneficial mutation is often slower than expected from its selective advantage.
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Leukemia patients carrying the ABL T315I mutation are often resistant to all available tyrosine kinase inhibitors, presenting the clinical challenge of finding effective treatment options.
Mono-allelic deletions (i.e., sole 17p deletion and sole 11q deletion) were often classified as functional, whereas mono-allelic mutations (i.e., sole TP53 mutation and sole ATM mutation) were often classified as p53-dysfunctional and ATM-dysfunctional, respectively.
Moreover, many neuroligin gene mutations were associated with autism, but the pathophysiological relevance of these mutations is often unknown, and their mechanisms of action uninvestigated.
The slow growth rate indicative of other Lmna/LMNA mutations is often accompanied by increased DNA damage [19] [21].
Frequency distribution of naturally occurring mutations is often associated with geographical and environmental factors able to affect genetic patterning and demography.
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