Figure 1.
Important genes in colorectal cancer development.
A) Key genes targeted in the various CRC phenotypes during development from precursor lesions to carcinomas. Genes in bold represent MAPK, PI3K, and TP53 signaling networks, and their mutation status have previously been determined [38]. B) The figure shows how part of the phosphatidyl inositol network interacts with the canonical PI3K pathway. Genes of which mutation status data are used for association analyses in the current paper are colored in blue, pink and brown. Abbreviations: GPCR, G-protein coupled receptor; RTK, receptor tyrosine kinase.
Figure 2.
Venn diagram displaying significantly deregulated signaling pathways in the AB and HuEx gene expression datasets.
The diagram shows that the results of the GSEA were highly reproducible with 33 and 49 pathways jointly up- and downregulated across the two datasets, respectively.
Table 1.
Significantly deregulated genes within the “Phosphatidylinositol signaling system”.
Figure 3.
Venn diagram displaying significantly deregulated genes within the “Phosphatidylinositol signaling system”.
Altogether 38 genes in the “Phosphatidylinositol signaling system” were altered in one or both dataset, eleven genes were found deregulated across both datasets.
Figure 4.
Boxplot showing markedly reduced expression levels of PLCD1 and PLCE1 in colorectal cancer.
The expression levels of PLCD1 and PLCE1 in CRC and colon cancer cell lines assessed by RT-PCR were significantly downregulated compared to normal colonic mucosa.
Table 2.
P-values for associations of PLCD1 and PLCE1 mRNA expression values with clinicopathological and mutation data.