Fig. 3 | Signal Transduction and Targeted Therapy

Fig. 3

From: KRAS mutation: from undruggable to druggable in cancer

Fig. 3

KRAS mutation in cancer. a The frequency of KRAS mutations across tumour types, including the mutation frequency of common sites and the subtype with the highest mutation rate in different tumour types. KRAS mutations are characterised by single-base missense mutations, 98% of which are found at codon 12, codon 13, or codon 61. Please refer to Table 1 for specific figures. b Specific mutant subtypes and percentages were represented in the top three cancers with the highest mutation rates of KRAS including pancreatic cancer, colorectal cancer, and nonsmall-cell lung cancer. c Frequency of co-occurring aberrations in KRAS mutant cells. Only a mutant prevalence of at least 3% is shown in addition to EGFR mutation, given the important effect of EGFR mutation on NSCLC. TP53: tumour protein p53 gene; DDR2: discoidin domain receptor tyrosine kinase 2 gene; MET: MNNG HOST Transforming gene; PIK3CA: phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha gene; STK11: serine/threonine kinase 11 gene; KEAP1: kelch-like ECH-associated protein 1 gene; ATM: ATM serine/threonine kinase gene, PIK3CG: phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit gamma gene; ERBB4: erb-b2 receptor tyrosine kinase 4 gene; KDR: kinase insert domain receptor gene; KIT: KIT proto-oncogene receptor tyrosine kinase gene; NFE2L2 nuclear factor erythroid 2, like 2 gene; PDGFR previous symbol of PDGFRB (platelet-derived growth factor receptor beta gene). Data acquired from The Cancer Genome Atlas (pan-Cancer) from cBioPortal

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