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The development and progression of colon carcinogenesis in both humans and rodents are known to be caused by the accumulation of cancer-related gene alterations, which results in their altered expression.
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In comparing the tolerant and sensitive NRAT1 genes, they found small but key sequence alterations, which resulted in a tolerant NRAT1 protein that effectively transported aluminum ions from the root cell wall into the cell, preventing aluminum toxicity that occurs in rice due to damage to the cell wall in the growing root tip.
3 The development of human PCa is associated with genetic or epigenetic alterations, which result in abnormal gene expression profiles.
We suggest that genetic alterations, which resulted in reduced viral recognition by antibodies generated against the 2009 pandemic influenza virus, underlie the return of the A(H1N1 pdm09 virus in 2013.
The mechanisms associated with decreased K. pneumoniae carbapenem susceptibility were likely due to the presence of cephalosporinases coupled with porin alterations, which resulted from the presence of the insertion sequences in the outer membrane encoding genes.
Cancer progression involves various cellular, morphological and molecular alterations which result in a transformed cellular phenotype, ultimately having the potential to invade surrounding tissue and disseminate throughout the body.
Although the precise molecular mechanisms of liver carcinogenesis are still unclear, the increased turnover of hepatocytes and inflammatory cell infiltrate seen in chronic hepatitis and cirrhosis may lead to an accumulation of molecular alterations, which ultimately result in the development of HCC.
Despite these benefits, there are some commonly occurring side effects of EGFR inhibitors (papulopustular rash, dry skin, itching, hair and periungual alterations), which can result in reduced quality of life as well as a reduction, interruption or discontinuation of cetuximab treatment.
Such studies will aid in understanding the nature of the alteration of ABL which results in the activation of its transforming potential.
Tolerance and the resultant withdrawal syndrome may be due to receptor down-regulation and GABAA receptor alterations in gene expression which results in long-term changes in the function of the GABAergic neuronal system.
Oncogenic transformation is often driven by the genetic alteration of protein kinases, which results in inappropriate activity of downstream transcription factors (TFs).
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