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This criticism has its background in studies where little overlap between gene expression alterations induced in the liver in vivo and in cultured hepatocytes has been reported (Kienhuis et al. 2009).
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As the relation between chromosome loss and gene expression alterations is complex, we must interpret the observed lack of gene expression differences between these groups cautiously in this context.
The comparison of gene expression alterations between various drugs opened a new means to classify the different psychoactive compounds and to predict their cellular targets; this is well exemplified in the case of tianeptine, an antidepressant with unknown mechanisms of action.
The relationship between three-dimensional chromosome organization and gene expression alterations underlying disease progression warrants further investigations.
Significant correlations between the degree of test compound-induced gene expression alterations in vivo and in vitro were obtained for the metabolism, stress and DNA repair associated genes at concentrations covering a range from cytotoxic to non-toxic/in vivo relevant concentrations (Fig. 44).
We have unveiled hitherto unknown interactions between mutated and methylated genes that are associated with gene expression alterations in HNSCC.
For example, studies comparing gene expression levels between tumor and healthy tissues will be able to identify tumor-specific gene expression alterations more confidently.
Also, MT gene expression alterations are associated with carcinogenesis and with aggressive tumour behaviour and even chemotherapy resistance11.
Particularly relevant in this regard is the substantial overlap between gene expression changes and alterations in SA content induced during an avirulent pathogen-triggered ETI response, and those induced by treatment with flg22, an 22-amino-acid epitope of the archetypal MAMP elicitor flagellin [ 8, 67, 68].
Our results contrast with those of Marella et al. [11], which showed a lack of correlation between gene expression and copy number alterations.
Cancer genes which are potential drivers (i.e. significant correlation between gene expression and copy number alterations) are highlighted in bold.
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