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The idea is to identify commonalities of gene combinations with differential expression patterns between cancer and corresponding control tissue across multiple cancer types, which could provide useful information about common underlying mechanisms of carcinogenesis of different cancers.
A total of 452 genes were found to be differentially expressed as determined using the following criteria: the expression levels in cancer and the corresponding control tissue show at least 2-fold change, and the statistical significance, P-value, of having this level of expression change is <0.05 (see Material and Methods; gene names are listed in Table S1).
Detection of p53, Waf-1, Bax and Bcl-2 in the corresponding control tissue was positive and strong, as expected.
Representative photographs of INPP4B, PTEN, PDPK1, and pAkt expression and corresponding control tissue are shown in Figure 1A L.
Supplementary material Fig. S2A shows increased Pdgfrβ mRNA and protein levels in total lung tissue homogenates of Sesn2 KO mice when compared with the corresponding control tissue.
Hematoxylin and eosin-stained tissue sections from ESCC, CSCC, and corresponding control tissue were reviewed by Professor Shen Zhongying from the Institute of Oncology Pathology to confirm the original findings and define representative tumor regions.
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For each k-gene combination among these genes, its classification accuracy between each cancer type and the corresponding control tissues was calculated.
In addition to individual gene markers, we have focused on gene combinations that can be used to distinguish multiple cancer types from their corresponding control tissues.
We have examined differentially expressed genes with at least 2-fold changes between cancer and corresponding control tissues across all seven cancer types and attempted to find those genes common to multiple cancer types.
The distributions of the fold-changes (FC) of individual genes across all genes between cancer and the corresponding control tissues for the seven types of cancers were checked and found to be highly similar.
The activation status of ADAM-12 and ADAMTS-1 in tumours and corresponding control tissues was investigated by Western blotting.
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Justyna Jupowicz-Kozak
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