Fig. 2
From: RAS signaling in carcinogenesis, cancer therapy and resistance mechanisms
The frequency of RAS mutations varies across different cancer types and is notably concentrated at the G12, G13, and Q61 residues in the exons of RAS oncogenes. (A) KRAS mutations are most prevalent in pancreatic ductal adenocarcinoma, followed by colorectal cancer and lung adenocarcinoma. (B) HRAS mutations are primarily observed in pheochromocytoma and paraganglioma, thymoma, and head and neck squamous cell carcinoma. (C) NRAS mutations are mainly found in skin cutaneous melanoma, acute myeloid leukemia, and thyroid carcinoma. (D) The prevalence of G12, G13, and Q61 mutations in the exons of KRAS, HRAS, and NRAS isoforms is highlighted. The data shown in graphs (A), (B), and (C) are sourced from the cBioPortal TCGA (available via the cBioPortal for Cancer Genomics), while the data in graph (D) were derived from recent studies utilizing the COSMIC or cBioPortal databases [3, 26, 27]