{"entity":{"id":"kras","kind":"target","name":"KRAS","aka":[],"tldr":"KRAS is the most commonly mutated cancer gene, called 'undruggable' for 40 years until 2021.","summary":"KRAS mutations drive ~90% of pancreatic, ~40% of colorectal, and ~30% of lung adenocarcinomas. Sotorasib and adagrasib (G12C) were first; G12D inhibitors (MRTX1133, zoldonrasib) and pan-RAS(ON) inhibitors (daraxonrasib, RMC-6236, in phase 3 in pancreatic cancer) are the next wave. Combination with EGFR antibodies is needed in colorectal cancer.","asOf":"2026-09-04","wikipedia":"https://en.wikipedia.org/wiki/KRAS","links":[{"label":"Wikipedia","url":"https://en.wikipedia.org/wiki/KRAS"}],"tags":["driver"],"related":["kras-g12d","kras-g12c","stk11-keap1-loss","ras-wild-type"],"cancers":["pancreatic","colorectal","nsclc","gallbladder"],"sections":[],"technologies":[],"targets":[],"drugs":["guardant360-cdx","therascreen-cdx","tempus-xt-cdx","resolution-ctdx-first","calderasib","jdq443","gfh375","setidegrasib","incb161734","vs-7375","jyp0015"],"companies":["adventris-pharmaceuticals","bridgebio-oncology-therapeutics","cogent-biosciences","erasca","imagene-ai","inivata","kumquat-biosciences","lucence","treeline-biosciences"],"institutions":[],"pathways":["ras-mapk","pi3k-akt-mtor","aml-signalling","chemical-carcinogenesis-receptor-activation","choline-metabolism-in-cancer","cml-signalling","colorectal-cancer-signalling","endometrial-cancer-signalling","gastric-cancer-signalling","hepatocellular-carcinoma-signalling","micrornas-in-cancer","nsclc-signalling","pancreatic-cancer-signalling","renal-cell-carcinoma-signalling","thyroid-cancer-signalling"],"terms":["kras-mutation-subtypes","wild-type"],"trials":["nct06385925","nct06667544","nct06243354"],"people":[],"bottlenecks":[],"keyPapers":["paper-singhi-targeted-genome-profiling-3594-pdac-gastroenterology-2019","paper-philip-kras-wild-type-pancreatic-ccr-2022","paper-witkiewicz-pancreatic-exomes-utsw-nat-commun-2015","paper-tcga-pancreatic-integrated-characterisation-cancer-cell-2017","paper-bournet-kras-g12d-prognosis-pancreatic-ctg-2016","paper-qian-driver-genes-outcomes-resected-pancreatic-jama-oncol-2018","paper-daraxonrasib-pancreatic-n-engl-j-med-2026","paper-codebreak-100-sotorasib-kras-g12c-pancreatic-nejm-2023","paper-krystal-1-adagrasib-kras-g12c-solid-tumours-jco-2023","paper-heining-nrg1-fusions-kras-wild-type-pancreatic-cancer-discov-2018","paper-jones-nrg1-fusions-recurrent-actionable-kras-wild-type-pdac-ccr-2019","paper-karapetis-kras-cetuximab-colorectal-nejm-2008","paper-vogelstein-genetic-alterations-colorectal-tumor-development-nejm-1988","paper-loree-tumour-location-continuum-colorectal-ccr-2018","paper-sepulveda-molecular-biomarkers-colorectal-guideline-jco-2017","paper-schirripa-kras-g12c-metastatic-colorectal-clin-colorectal-cancer-2020","paper-codebreak-300-nejm-2023","paper-krystal-1-crc-yaeger-nejm-2023","paper-douillard-prime-panitumumab-ras-nejm-2013","paper-giraldo-gallbladder-msk-impact-ccr-2022","paper-li-gallbladder-exome-erbb-nat-genet-2014","paper-suryavanshi-indian-gallbladder-genomics-jco-go-2025","paper-javle-biliary-ngs-cancer-2016","paper-kris-lung-cancer-mutation-consortium-jama-2014","paper-alexandrov-tobacco-smoking-mutational-signatures-science-2016"],"journals":[],"dependsOn":[],"notes":["Pancreatic ductal adenocarcinoma: mutated in 88 to 94% (88% of 3,594 on targeted panels, Singhi 2019; 93.7% of 2,336 MSK-IMPACT samples, cBioPortal). The allele matters: G12D about 40%, G12V about 32%, G12R about 16%, Q61 about 7% and G12C 1 to 2%. G12D carries the worst survival (6 versus 9 months; Bournet 2016) and G12R the best; codon 61 alleles were associated with improved survival (Witkiewicz 2015). Mutant allele copy gain is common (296 of 853 dosage-annotated MSK samples) and helps set the basal-like phenotype (Chan-Seng-Yue 2020). Daraxonrasib, a tri-complex RAS(ON) inhibitor, halved the death hazard in previously treated RAS-mutant disease (RASolute 302; O'Reilly 2026), while the G12C-only covalent inhibitors reach 21 to 33% response in the 1 to 2% who carry that allele (Strickler 2023, Bekaii-Saab 2023).","Colorectal cancer: mutated in 40 to 44%, with an allele distribution unlike any other cancer: G12D about 29%, G12V about 20%, G13D about 18%, G12C about 7% and A146T about 6% of KRAS mutation records (cBioPortal). About one in six KRAS mutations sits outside exon 2, which is why extended RAS testing of KRAS and NRAS exons 2, 3 and 4 is required before an EGFR antibody (Douillard 2013, Sepulveda 2017). Any RAS mutation predicts no benefit from cetuximab or panitumumab (Karapetis 2008); G12C, about 3% of all colorectal cancers, is the only allele with a targeted option, and only in combination with an EGFR antibody because the inhibitor alone triggers adaptive EGFR reactivation. KRAS-mutant subclones are also the commonest cause of acquired resistance to EGFR antibodies and are visible in plasma months before progression (Misale 2012, Diaz 2012).","Lung cancer: mutated in 27 to 33% of Western adenocarcinoma, 10.9% in East Asian adenocarcinoma and 7.3% in never smokers, and in only 1.4% of squamous tumours (cBioPortal). Lung is the one common cancer where G12C dominates, at 41 to 51% of KRAS mutation records or about 13% of all adenocarcinomas, because the G to T transversion that produces it is the signature lesion of tobacco carcinogens (Alexandrov 2016); in colorectal and pancreatic cancer G12D leads instead. The other half of the KRAS population, G12V, G12D, G12A, G13X and Q61X, has no approved inhibitor. What decides behaviour is the co-mutation rather than the allele: STK11 loss makes the tumour immune-poor, KEAP1 loss makes it resistant to everything, and TP53 co-mutation makes it inflamed and relatively favourable (Skoulidis 2015, Arbour 2018, Ricciuti 2022)."],"symbol":"KRAS","role":[],"sources":[],"specificity":"tumour-specific","distribution":"many-types","specificityNote":"Tumour-specific alteration: 2 of 2 label readouts filed under it measure a sequence variant (KRAS G12C, KRAS G12D (and other non-G12C KRAS mutations)) absent from normal cells. HPA KRAS: RNA low tissue specificity; high antibody staining in 7 normal tissues; highest cancer staining ovarian cancer (2 of 9 high). Distribution: 6 cancer families in the corpus carry a prevalence row, label threshold or catalogue link for it (Colorectal cancer, Lung cancer (all types), Pancreatic ductal adenocarcinoma, Biliary tract cancer (all types), Endometrial cancer, Ovarian cancer); Open Targets associates it with 24 specific cancer types at or above 0.5 (non-small cell lung carcinoma, gastric cancer, acute myeloid leukemia, linear nevus sebaceous syndrome, lung adenocarcinoma, urinary bladder cancer and more). (Rule 3 of scripts/fetch-target-specificity.ts.)","specificitySources":[{"label":"KRAS G12C label threshold","url":"https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=c80a362c-7ac3-4894-a076-0691e68ef8c1","note":"KRAS G12C"},{"label":"KRAS G12D (and other non-G12C KRAS mutations) label threshold","url":"https://www.fda.gov/medical-devices/in-vitro-diagnostics/list-cleared-or-approved-companion-diagnostic-devices-in-vitro-and-imaging-tools","note":"KRAS wild-type (negative selector)"},{"label":"Human Protein Atlas KRAS tissue","url":"https://www.proteinatlas.org/ENSG00000133703-KRAS/tissue","note":"RNA tissue and blood lineage specificity, normal tissue antibody staining (version 25.1, CC BY-SA 3.0)"},{"label":"Open Targets ENSG00000133703 associations","url":"https://platform.opentargets.org/target/ENSG00000133703/associations","note":"cancer associations at or above 0.5 (CC0)"}],"hgnc":"HGNC:6407","ensembl":"ENSG00000133703","uniprot":"P01116","entrez":"3845","firstDescribed":1983,"firstDescribedBasis":"sequence","firstDescribedNote":"Earliest sequence paper UniProt cites for the protein: McGrath J.P. et al, Nature, 1983, \"Structure and organization of the human Ki-ras proto-oncogene and a related processed pseudogene\".","firstDescribedSource":"https://pubmed.ncbi.nlm.nih.gov/6308466/","biology":"Small GTPase switch; oncogenic mutations lock it in the GTP-bound ON state. Adaptive feedback and secondary mutations drive resistance.","whereFound":["Pancreatic (~90%)","Colorectal (~40-45%)","Lung adenocarcinoma (~30%)","Endometrial, ovarian (subsets)","Pancreatic ductal adenocarcinoma: activating mutation (any allele) 88-94%","Pancreatic ductal adenocarcinoma: g12d allele (share of kras mutation records) 39-41%","Pancreatic ductal adenocarcinoma: g12v allele (share of kras mutation records) 28-37%","Pancreatic ductal adenocarcinoma: g12r allele (share of kras mutation records) 12-21%","Pancreatic ductal adenocarcinoma: q61h, q61r, q61l or q61k allele (share of kras mutation records) 5-8%","Pancreatic ductal adenocarcinoma: g12c allele (share of kras mutation records) 1-2%","Pancreatic ductal adenocarcinoma: no kras mutation (fusion and alternative-driver search) 6-12%","Colorectal cancer: activating mutation (any allele) 40-44%","Colorectal cancer: g12d allele (share of kras mutation records) 27-29%","Colorectal cancer: g12v allele (share of kras mutation records) 16-22%","Colorectal cancer: g13d allele (share of kras mutation records) 16-24%","Colorectal cancer: g12c allele (share of kras mutation records) 6-9%","Colorectal cancer: codon 59, 61, 117 or 146 mutation (share of kras missense records) 16-18%","Gallbladder cancer: mutation (amplification rarer) about 11%","Non-small-cell lung cancer: activating mutation (any allele) 27-33%","Non-small-cell lung cancer: g12c allele (share of kras mutation records) 41-51%","Non-small-cell lung cancer: g12v, g12d, g12a, g13x and q61x (share of kras mutation records) 49-59%"],"targetClass":"oncogene","prevalence":[{"cancerId":"pancreatic","pct":"85-90","measure":"Any KRAS mutation","source":"https://www.cbioportal.org/study/summary?id=paad_tcga_pan_can_atlas_2018","note":"G12D ~40%, G12V ~30%, G12R ~15%, G12C ~1-2%"},{"cancerId":"colorectal","pct":"40-45","measure":"Any KRAS mutation","source":"https://www.cbioportal.org/study/summary?id=coadread_tcga_pan_can_atlas_2018","note":"G12C ~3-4%"},{"cancerId":"nsclc","pct":"25-30","measure":"Adenocarcinoma, any KRAS mutation","source":"https://www.cbioportal.org/study/summary?id=luad_tcga_pan_can_atlas_2018","note":"G12C ~13% of adenocarcinoma"},{"cancerId":"endometrial","pct":"15-20","measure":"Any KRAS mutation","source":"https://www.cbioportal.org/study/summary?id=ucec_tcga_pan_can_atlas_2018"},{"cancerId":"ovarian","pct":"10-15","measure":"Low-grade serous and mucinous","source":"https://www.cbioportal.org/study/summary?id=ov_tcga_pan_can_atlas_2018"},{"cancerId":"pancreatic","pct":"88-94","measure":"Activating mutation (any allele)","source":"https://doi.org/10.1053/j.gastro.2019.02.037","note":"88% of 3,594 targeted-panel samples (Singhi 2019); 2,217 of 2,483, 89.3%, in the Caris cohort (Philip 2022); more than 90% of 109 microdissected exomes (Witkiewicz 2015); cBioPortal: 2,188 of 2,336, 93.7%, in pdac_msk_2024; 361 of 395, 91.4%, in pancreas_msk_2024; 135 of 140, 96.4%, in paad_cptac_2021; 344 of 383, 89.8%, in paad_qcmg_uq_2016; 100 of 109, 91.7%, in paad_utsw_2015; 94 of 99, 94.9%, in paad_icgc. A subset of tumours carries multiple KRAS mutations, some biallelic (Cancer Genome Atlas 2017); mutant KRAS copy gains were recorded in 296 of 853 dosage-annotated pdac_msk_2024 samples (2 or more extra copies in 201, 3 or more in 95)."},{"cancerId":"pancreatic","pct":"39-41","measure":"G12D allele (share of KRAS mutation records)","source":"https://www.cbioportal.org/study/summary?id=pdac_msk_2024","note":"889 of 2,188 KRAS mutation records, 40.6%, in pdac_msk_2024 (the study's own KRAS_VARIANT attribute: 892 G12D, 706 G12V, 352 G12R, 111 Q61H, 37 Q61R, 26 G12C, 70 other); 136 of 344, 39.5%, in paad_qcmg_uq_2016; 61 of 135, 45.2%, in paad_cptac_2021; 39 of 95, 41.1%, in paad_icgc; 49 of 119, 41.2%, in paad_tcga_pan_can_atlas_2018; 37 of 100, 37.0%, in paad_utsw_2015 (cBioPortal). Among 219 advanced patients genotyped on EUS-guided biopsies, G12D 73, G12V 53, G12R 21 (Bournet 2016)."},{"cancerId":"pancreatic","pct":"28-37","measure":"G12V allele (share of KRAS mutation records)","source":"https://www.cbioportal.org/study/summary?id=pdac_msk_2024","note":"709 of 2,188, 32.4%, in pdac_msk_2024; 108 of 344, 31.4%, in paad_qcmg_uq_2016; 40 of 135, 29.6%, in paad_cptac_2021; 35 of 95, 36.8%, in paad_icgc; 33 of 119, 27.7%, in paad_tcga_pan_can_atlas_2018; 40 of 100, 40.0%, in paad_utsw_2015 (cBioPortal, mutation records). 53 of 147 codon-12 mutations in 219 advanced patients (Bournet 2016)."},{"cancerId":"pancreatic","pct":"12-21","measure":"G12R allele (share of KRAS mutation records)","source":"https://www.cbioportal.org/study/summary?id=pdac_msk_2024","note":"354 of 2,188, 16.2%, in pdac_msk_2024; 61 of 344, 17.7%, in paad_qcmg_uq_2016; 23 of 135, 17.0%, in paad_cptac_2021; 16 of 95, 16.8%, in paad_icgc; 25 of 119, 21.0%, in paad_tcga_pan_can_atlas_2018; 12 of 100, 12.0%, in paad_utsw_2015 (cBioPortal, mutation records). G12R is almost unique to pancreatic cancer among KRAS-driven tumours and carried the longest survival of the codon-12 alleles, 14 months, in 219 advanced patients (Bournet 2016)."},{"cancerId":"pancreatic","pct":"5-8","measure":"Q61H, Q61R, Q61L or Q61K allele (share of KRAS mutation records)","source":"https://www.cbioportal.org/study/summary?id=pdac_msk_2024","note":"167 of 2,188, 7.6% (Q61H 107, Q61R 38, Q61L 14, Q61K 8), in pdac_msk_2024; 23 of 344, 6.7% (Q61H 19), in paad_qcmg_uq_2016; 8 of 135, 5.9%, in paad_cptac_2021; 5 of 95, 5.3%, in paad_icgc; 8 of 119, 6.7%, in paad_tcga_pan_can_atlas_2018; 7 of 100, 7.0%, in paad_utsw_2015 (cBioPortal, mutation records). Codon 61 alleles were selectively associated with improved survival among 109 microdissected cancers (Witkiewicz 2015)."},{"cancerId":"pancreatic","pct":"1-2","measure":"G12C allele (share of KRAS mutation records)","source":"https://doi.org/10.1056/NEJMoa2208470","note":"About 1 to 2% of pancreatic cancers (Strickler 2023); 28 of 2,188 KRAS mutation records, 1.3%, and 26 of 2,194 samples with a KRAS_VARIANT call, 1.2%, in pdac_msk_2024; 6 of 344, 1.7%, in paad_qcmg_uq_2016; 4 of 100, 4.0%, in paad_utsw_2015; 3 of 361 in pancreas_msk_2024; 1 of 135 in paad_cptac_2021; 1 of 119 in paad_tcga_pan_can_atlas_2018 (cBioPortal). CodeBreaK 100 treated 38 previously treated patients: 8 centrally confirmed responses, 21%, progression-free survival 4.0 months, overall survival 6.9 months (Strickler 2023); KRYSTAL-1 gave 7 of 21 pancreatic responses, 33.3%, to adagrasib (Bekaii-Saab 2023)."},{"cancerId":"pancreatic","pct":"6-12","measure":"No KRAS mutation (fusion and alternative-driver search)","source":"https://doi.org/10.1158/1078-0432.CCR-21-3581","note":"266 of 2,483, 10.7% (Philip 2022); 12% of 3,594 (Singhi 2019); 148 of 2,336, 6.3%, in pdac_msk_2024; 39 of 383, 10.2%, in paad_qcmg_uq_2016; 5 of 99 by the study's KRAS_MUTATION attribute in paad_icgc; 34 of 395, 8.6%, in pancreas_msk_2024 (cBioPortal). Among KRAS wild-type tumours: TP53 mutated in 44.5%, BRAF in 13.0%, fusions of BRAF 6.6%, FGFR2 5.2%, ALK 2.6%, RET 1.3% and NRG1 1.3%, amplification of FGF3 3%, ERBB2 2.2%, FGFR3 1.8%, NTRK 1.8% and MET 1.3%; MSI-high 4.7% against 0.7% and TMB-high 4.5% against 1% in KRAS-mutant disease (Philip 2022). KRAS wild-type TCGA tumours carried GNAS, BRAF, CTNNB1 and other RAS-pathway alterations (Cancer Genome Atlas 2017); all 4 of 17 young adults (Heining 2018) and all 3 of 47 patients (Jones 2019) with wild-type tumours carried a kinase or NRG1 fusion on whole-genome sequencing."},{"cancerId":"colorectal","pct":"40-44","measure":"Activating mutation (any allele)","source":"https://www.cbioportal.org/study/summary?id=crc_msk_2026","note":"cBioPortal: 3,096 of 7,237, 42.8%, in crc_msk_2026; 495 of 1,134, 43.7%, in crc_msk_2017; 666 of 1,516, 43.9%, in crc_eo_2020; 218 of 534, 40.8%, in coadread_tcga_pan_can_atlas_2018; 94 of 224, 42.0%, in coadread_tcga_pub; 173 of 619, 27.9%, in coadread_dfci_2016; 239 of 1,015, 23.5%, in crc_sysucc_2022. In CO.17, 42.3% of 394 evaluable tumours carried a K-ras exon 2 mutation (Karapetis 2008); ras-gene mutations were present in 58% of adenomas larger than 1 cm but only 9% of adenomas under 1 cm (Vogelstein 1988)."},{"cancerId":"colorectal","pct":"27-29","measure":"G12D allele (share of KRAS mutation records)","source":"https://www.cbioportal.org/study/summary?id=crc_msk_2026","note":"cBioPortal, mutation records: 908 of 3,169, 28.7%, in crc_msk_2026; 137 of 504, 27.2%, in crc_msk_2017; 191 of 680, 28.1%, in crc_eo_2020; 58 of 223, 26.0%, in coadread_tcga_pan_can_atlas_2018; 45 of 177, 25.4%, in coadread_dfci_2016; 73 of 243, 30.0%, in crc_sysucc_2022."},{"cancerId":"colorectal","pct":"16-22","measure":"G12V allele (share of KRAS mutation records)","source":"https://www.cbioportal.org/study/summary?id=crc_msk_2026","note":"cBioPortal, mutation records: 622 of 3,169, 19.6%, in crc_msk_2026; 101 of 504, 20.0%, in crc_msk_2017; 140 of 680, 20.6%, in crc_eo_2020; 49 of 223, 22.0%, in coadread_tcga_pan_can_atlas_2018; 24 of 177, 13.6%, in coadread_dfci_2016; 38 of 243, 15.6%, in crc_sysucc_2022."},{"cancerId":"colorectal","pct":"16-24","measure":"G13D allele (share of KRAS mutation records)","source":"https://www.cbioportal.org/study/summary?id=crc_msk_2026","note":"cBioPortal, mutation records: 569 of 3,169, 18.0%, in crc_msk_2026; 90 of 504, 17.9%, in crc_msk_2017; 118 of 680, 17.4%, in crc_eo_2020; 37 of 223, 16.6%, in coadread_tcga_pan_can_atlas_2018; 43 of 177, 24.3%, in coadread_dfci_2016; 55 of 243, 22.6%, in crc_sysucc_2022."},{"cancerId":"colorectal","pct":"6-9","measure":"G12C allele (share of KRAS mutation records)","source":"https://www.cbioportal.org/study/summary?id=crc_msk_2026","note":"cBioPortal, mutation records: 219 of 3,169, 6.9%, in crc_msk_2026; 32 of 504, 6.3%, in crc_msk_2017; 42 of 680, 6.2%, in crc_eo_2020; 15 of 223, 6.7%, in coadread_tcga_pan_can_atlas_2018; 16 of 177, 9.0%, in coadread_dfci_2016; 13 of 243, 5.3%, in crc_sysucc_2022. That is about 3% of all colorectal cancers. Among 839 KRAS-mutant metastatic patients, 145, 17%, carried G12C, more often men and with lung and liver metastases, and their overall survival was shorter than with other KRAS alleles (hazard ratio 1.32) (Schirripa 2020)."},{"cancerId":"colorectal","pct":"16-18","measure":"Codon 59, 61, 117 or 146 mutation (share of KRAS missense records)","source":"https://www.cbioportal.org/study/summary?id=crc_msk_2026","note":"cBioPortal, missense records: 491 of 3,155, 15.6%, in crc_msk_2026 (codons 59 and 61, 152; codons 117 and 146, 270; other, 69); 85 of 503, 16.9%, in crc_msk_2017; 17 of 93, 18.3%, in coadread_tcga_pub; 104 of 676, 15.4%, in crc_eo_2020. A146T alone is 185 of 3,169 KRAS records in crc_msk_2026 and 33 of 504 in crc_msk_2017."},{"cancerId":"gallbladder","pct":11,"measure":"Mutation (amplification rarer)","source":"https://doi.org/10.1158/1078-0432.ccr-22-1954","note":"11% of 244 samples (Giraldo 2022; cBioPortal gbc_mskcc_2022: mutation in 18 of 244, 7.4%, and amplification in 10 of 244, 4.1%); 7.8% of 57 (Li 2014); 7% of 376 Indian patients (Suryavanshi 2025); 7.8% of 103 samples in cBioPortal gbc_msk_2018."},{"cancerId":"nsclc","pct":"27-33","measure":"Activating mutation (any allele)","source":"https://www.cbioportal.org/study/summary?id=luad_mskcc_2023_met_organotropism","note":"cBioPortal: 787 of 2,653, 29.7%, in luad_mskcc_2023_met_organotropism; 241 of 915, 26.3%, in lung_msk_2017; 168 of 566, 29.7%, in luad_tcga_pan_can_atlas_2018; 75 of 230, 32.6%, in luad_tcga_pub; 33 of 110, 30.0%, in luad_cptac_2020; 33 of 302, 10.9%, in luad_oncosg_2020; 17 of 232, 7.3%, in lung_nci_2022. The Lung Cancer Mutation Consortium found KRAS in 182 of 733 fully genotyped adenocarcinomas, 25%, the commonest single driver in that series (Kris 2014)."},{"cancerId":"nsclc","pct":"41-51","measure":"G12C allele (share of KRAS mutation records)","source":"https://www.cbioportal.org/study/summary?id=luad_mskcc_2023_met_organotropism","note":"cBioPortal, mutation records: 344 of 797, 43.2%, in luad_mskcc_2023_met_organotropism; 268 of 526, 50.9%, in nsclc_ctdx_msk_2022; 104 of 244, 42.6%, in lung_msk_2017; 70 of 172, 40.7%, in luad_tcga_pan_can_atlas_2018; 96 of 224, 42.9%, in nsclc_tcga_broad_2016; 36 of 87, 41.4%, in nsclc_pd1_msk_2018. That is about 13% of all lung adenocarcinomas (344 of 2,653 samples in luad_mskcc_2023_met_organotropism)."},{"cancerId":"nsclc","pct":"49-59","measure":"G12V, G12D, G12A, G13X and Q61X (share of KRAS mutation records)","source":"https://www.cbioportal.org/study/summary?id=luad_mskcc_2023_met_organotropism","note":"cBioPortal, mutation records in luad_mskcc_2023_met_organotropism: G12V 119 of 797 (14.9%), G12D 97 (12.2%), G12A 72 (9.0%), G13C 32 (4.0%), Q61H 30 (3.8%), G13D 30 (3.8%), G12R 11, G12S 10, G12F 6, Q61L 6. In lung_msk_2017: G12D 37 of 244 (15.2%), G12V 37 (15.2%), G12A 19, G13D 12, Q61H 11."}]},"route":"/targets/kras/","neighbours":{"biomarker":[{"id":"kras-g12c","kind":"biomarker","name":"KRAS G12C","route":"/biomarkers/kras-g12c/"},{"id":"kras-g12d","kind":"biomarker","name":"KRAS G12D (and other non-G12C KRAS mutations)","route":"/biomarkers/kras-g12d/"},{"id":"ras-wild-type","kind":"biomarker","name":"RAS wild-type (extended KRAS and NRAS testing)","route":"/biomarkers/ras-wild-type/"},{"id":"stk11-keap1-loss","kind":"biomarker","name":"STK11 or KEAP1 loss in KRAS-mutant lung adenocarcinoma","route":"/biomarkers/stk11-keap1-loss/"}],"cancer":[{"id":"lung-adenocarcinoma","kind":"cancer","name":"Adenocarcinoma of the lung","route":"/cancers/lung-adenocarcinoma/"},{"id":"pancreatic-adenosquamous-carcinoma","kind":"cancer","name":"Adenosquamous carcinoma of the 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