Fig 1: Comparison of RNF215 expression in the KRAS, NRAS, BRAF and PIK3CA mutant vs. WT colorectal cancer groups via the TIMER 2.0 database. (A) Expression of RNF215 in KRAS mutant vs. WT colon cancer (P=0.84). (B) Expression of RNF215 in KRAS mutant vs. WT rectal cancer (P=0.081). (C) Expression of RNF215 in NRAS mutant vs. WT colon cancer (P=0.79). (D) Expression of RNF215 in NRAS mutant vs. WT rectal cancer (P=0.12). (E) Expression of RNF215 in BRAF mutant vs. WT colon cancer (P=0.0017). (F) Expression of RNF215 in BRAF mutant vs. WT rectal cancer (P=0.019). (G) Expression of RNF215 in PIK3CA mutant vs. WT colon cancer (P=0.88). (H) Expression of RNF215 in PIK3CA mutant vs. WT rectal cancer (P=0.37). RNF215, ring finger protein 215; WT, wild-type.
Fig 2: Analysis of concomitant mutations in KRAS, NRAS, BRAF and PIK3CA. (A) Venn diagram showing the distribution of single and concomitant mutations in the KRAS, NRAS, BRAF and PIK3CA genes. (B) Frequency of mutations in KRAS, NRAS, BRAF and PIK3CA exons in patients with CRC. The mutations in all exons are listed in the figure. Among them, the frequency of KRAS exon 2 mutations was the highest (55.8%), and concomitant mutations accounted for 7.7% (8/104) of mutations.
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