KRAS

Overview

KRAS is a canonical RAS-family oncogene and one of the most frequently mutated drivers in human cancer, with prominent roles in LUAD, colorectal, and pancreatic cancers.

Alterations observed in the corpus

  • Advanced NSCLC: detection of pathogenic KRAS alterations in ctDNA (vs tissue only) was associated with worse prognosis in the prospective ctDx Lung cohort (n=1,127) PMID:36357680.
  • Appendiceal adenocarcinoma: KRAS/NRAS mutations in the absence of GNAS and TP53 alterations mark the clinically indolent RAS-mut predominant MAAP subtype with lowest mutational and chromosomal burden and best OS PMID:36493333.
  • Histiocytosis: KRAS mutated in 7% of profiled cases; one case had co-occurring KRAS G12D and BRAF D594H PMID:36862133.
  • Female germ cell tumors: KRAS among oncogenic mutations observed in a minority of cases PMID:36862133.
  • LUAD metastasis: KRAS G12C elevated (21%) in primaries that metastasized to liver vs the matched liver lesions (6%, p<0.001); mutually exclusive with EGFR PMID:37084736.
  • NSCLC brain metastases: KRAS commonly shared (truncal) between BM and matched primary or extracranial metastasis PMID:37591896.
  • KRAS was included in LUAD pathway/metastasis analyses in MSK-CHORD (n=24,950) PMID:39506116.
  • KRAS alterations characterized “biliary-class” intrahepatic cholangiocarcinoma (along with SMAD4 and CDKN2A loss), associated with markedly worse OS PMID:38864854.
  • In 1,360 resected PAAD patients at MSK (pancreas_msk_2024, 397 sequenced on MSK-IMPACT), KRAS was altered in 90%; allele distribution G12D 36.5% / G12V 32.5% / G12R 13.9% / other 8.1% / WT 9.1%. KRASG12R was enriched in stage I (23% vs 11% in stage II–III, p=0.022), more often node-negative (47% vs 26% for G12D, p=0.019), and associated with improved OS and decreased distant recurrence; bulk RNA-seq (n=100) and CosMx SMI spatial profiling (n=20) identified enhanced KRAS signaling / EMT in KRASG12D tumors and increased TNF/NF-κB signaling in KRASG12R; isogenic KrasG12R/+;Trp53KO mouse PDAC organoids recapitulated reduced migration and improved orthotopic survival PMID:39214094.
  • KRAS mutations were detected in CSF ctDNA from NSCLC patients with CNS involvement in the csf_msk_2024 cohort (1,007 CSF samples, 711 patients); KRAS appeared as an off-target resistance alteration in EGFR-mutant patients PMID:39289779.
  • Cervical cancer: KRAS mutations in 12% of 177 MSK patients; enriched in gastric-type adenocarcinoma (27%) and UEA (20%); includes 1 G12C hotspot mutation; significantly enriched vs TCGA (P=0.019). KRAS G12C inhibitors (adagrasib, sotorasib) considered therapeutically relevant PMID:37643132.
  • Rhabdomyosarcoma: KRAS is one of the RAS/PIK3CA pathway alterations found in 5/17 FN-RMS patients in a sequential genomic analysis of 35 tumor pairs PMID:37730754.
  • Hepatocellular carcinoma: KRAS detected as cfDNA-exclusive alteration in one of 37 paired plasma-tissue samples from 51 advanced HCC patients; classified as OncoKB level 4 PMID:37769223.
  • HER2-positive esophagogastric cancer: KRAS oncogenic alterations associated with inferior PFS on univariate analysis; identified as a resistance mechanism in escape lesions from combined pembrolizumab + trastuzumab + chemotherapy (MSK cohort, n=226) PMID:37406106.
  • Endometrial carcinoma: KRAS oncogenic alterations less frequent in Black patients (12% vs 21% in White patients); the difference is driven by fewer endometrioid ECs in Black patients (MSK, 259 Black vs 1,276 White EC patients) PMID:37651310.
  • Esophagogastric cancer (early-onset vs average-onset): KRAS oncogenic alterations trend toward higher frequency in average-onset (15% vs 12%, P=0.23); not significantly different PMID:37699004.
  • dMMR gynecologic cancers: KRAS mutated in 24% of the nivolumab phase 2 trial cohort (n=35 MSI-H patients; 26% responders, 21% non-responders) — no significant association with nivolumab response PMID:38653864.
  • Pan-cancer liquid biopsy VTE risk: KRAS ctDNA detection carries adjusted HR = 1.65 (95% CI: 1.30-2.09; n=465) for venous thromboembolism in MSK multi-cancer cohort PMID:39147831.
  • KRAS mutation status (SNaPshot PCR, exon 2 codons 12/13) was annotated for 205/211 resected early-stage NSCLC patients in the Stanford NSCLC-Radiogenomics cohort as part of a paired radiogenomic dataset; per-subject status is provided as a data record rather than aggregate frequencies PMID:30325352.
  • In 2,336 MSK PDAC patients sequenced with MSK-IMPACT (pdac_msk_2024), KRAS was mutated in 95%; allele distribution G12D 41%, G12V 32%, G12R 16%, G12C 1%. Mutant-allele dosage gains (shallow gains, CNLOH, LOH, amplifications) were present in 42% of KRAS-mutant tumors and predict shorter OS independent of clinical stage (non-WGD HR_adj = 1.7, CI 1.4–2.0, P = 3.5×10⁻⁷). KRASG12R had better OS than G12D (HR_adj = 0.78, CI 0.67–0.92, P = 0.003). PMID:39753968
  • KRAS detected at 5.6% in cfDNA (numerically higher than matched tumor 3.7%) among metastatic urothelial carcinoma patients in the CALGB 90601 cfDNA cohort (MSK-ACCESS, n=201). PMID:40256659
  • Frequent mutations in LUAD correlating with smoking (P=0.021); copy number gain and increased expression in mutant tumours; mutually exclusive with EGFR mutations (P<1e-7). PMID:18948947
  • KRASG12C is the primary driver mutation in CRC; KRASG12C amplification (>20 copies) and secondary KRAS mutations (G12, H95, Y96, R68 positions) emerge as resistance mechanisms to combined KRASG12C + EGFR inhibition PMID:36355783
  • KRAS G12V mutation engineered in the A1309 CRC cell model used for FBXO7 synthetic lethality screening PMID:36334560
  • KRAS GOF mutations in 7% and amplifications in 4% of gallbladder carcinoma (GBC); KRAS p.G12C present in 2 patients (OncoKB level 3A) PMID:36228155
  • KRAS mutations were detected in prostate cancer by integrative genomic profiling of the MSKCC cohort PMID:20579941
  • KRAS mutations were identified in pancreatic neuroendocrine tumors (PANETs) by exome sequencing, though at lower frequency than in pancreatic ductal adenocarcinoma PMID:21252315
  • KRAS mutations were among somatic alterations identified in HGSOC by TCGA integrated genomic analysis of ovarian carcinoma PMID:21720365
  • KRAS is recurrently mutated in pancreatic cystic neoplasms by whole-exome sequencing, co-occurring with GNAS and RNF43 mutations in IPMNs PMID:22158988
  • KRAS mutation status is among the top genomic predictors of MEK inhibitor sensitivity in the CCLE pharmacogenomic profiling of 947 cancer cell lines PMID:22460905
  • Fusion events observed in TNBC WGS cohort (BCCRC, 65 tumors) PMID:22495314
  • Rare amplification event (<1% of patients) identified through the CNA-expression landscape in METABRIC (2,000 tumors); potentially relevant for tyrosine kinase inhibitor targeting PMID:22522925
  • Identified as a driver mutation gene in breast cancer WES of 100 tumors (Sanger cohort); KRAS mutations observed in tumour types beyond its canonical context PMID:22722201
  • Somatic mutations detected in TCGA colorectal adenocarcinoma cohort (276 tumors) PMID:22810696
  • KRAS mutations common in lung adenocarcinoma are essentially absent in lung squamous cell carcinoma (178 tumors, TCGA) PMID:22960745
  • Activating mutations in 27% of 183 LUAD cases; anti-correlated with EGFR mutations (P = 3.3e-4) PMID:22980975
  • Significantly mutated and amplified in 13% (10/74) of colorectal cancers (Genentech WES); co-occurs with RSPO fusions PMID:22895193
  • Copy-number amplification (32% of cases) in Basal-like breast cancer; not typically mutated in breast cancer, contrasting with other tumor types PMID:23000897
  • Activating mutations in 93% of pancreatic ductal adenocarcinoma cases (ICGC, 142 tumors); canonical GTPase/MAPK pathway driver PMID:23103869
  • Activating mutations in near haploid ALL as part of RTK/Ras signaling pathway (70.6% of near haploid cases affected by combined RTK/Ras alterations; St. Jude, 44 tumors) PMID:23334668
  • Novel CLL driver candidate; mutations at highly conserved sites identified in CLL WES of 160 tumors (Broad) PMID:23415222
  • Mutated in 5/145 (3%) of esophageal adenocarcinomas (EAC); 3 mutations at canonical p.G12 plus p.K117N (known transforming allele); KRAS/BRAF pathway mutations are uncommon in EAC contrasting with colorectal cancer PMID:23525077
  • Part of the non-FLT3 activated signaling gene subgroup in AML (with KIT, NRAS, PTPN11); contributes to the 59% signaling-pathway prevalence; activating mutations also implicated in alternative WNT/β-catenin activation in endometrial cancer (53% in POLE-ultramutated subgroup; mutually exclusive with CTNNB1 and SOX17) PMID:23634996
  • Mutated in 53% of POLE-ultramutated endometrial tumors; activating mutations implicated in WNT/β-catenin pathway activation; mutually exclusive with CTNNB1 and SOX17; molecular profiling of KRAS status contributed to reclassification of histologically ambiguous high-grade endometrial cases PMID:23636398
  • Non-hotspot compound mutations on the same allele in 2 pilocytic astrocytoma cases (E63K/R73M; L19F/Q22K), distinct from classical codon 12/13/61 hotspots; functional significance remains to be characterized PMID:23817572
  • Mutation in ~4% of high-grade urothelial bladder carcinoma (BLCA) as part of the MAPK-pathway alteration set (35% combined); mutual exclusivity with other RTK/RAS/RAF alterations suggests overlapping phenotypic effects PMID:23897969
  • Centered as the key driver in a co-clinical trial in KRAS-mutant LUAD testing selumetinib plus docetaxel; murine GEM arm delivered predictive response data and surfaced STK11 loss as a genetic modifier of response, informing retrospective reanalysis of the parallel human phase II study PMID:23999436
  • Confirmed recurrent driver mutation in transitional cell carcinoma (BLCA) by whole-exome sequencing of 99 Chinese TCC tumors; one of 7 previously known bladder cancer driver genes validated in the 37-significantly-mutated-gene analysis PMID:24121792
  • Single hotspot mutation detected in IHCH discovery screen; additional KRAS hits in prevalence screen confirm RAS signaling involvement in intrahepatic cholangiocarcinoma PMID:24185509
  • Wild-type in all 23 pancreatic carcinomas with acinar differentiation (0/23), contrasting sharply with PDAC where KRAS mutation is near-universal PMID:24293293
  • Gain-of-function mutation identified in ovarian mixed neuroendocrine-non-neuroendocrine neoplasm (MiNEN) PN19 in a WGTA study of rare metastatic neuroendocrine neoplasms PMID:24326773
  • KRAS codon 12/13 oncogenic hotspot mutations recurrently detected in multiple myeloma (MM), particularly enriched in previously treated patients; mutations frequently subclonal and co-mutation with BRAF was rarely simultaneously clonal PMID:24434212
  • KRAS codon 12/13/61 oncogenic hotspot mutations detected in rhabdomyosarcoma (RMS), predominantly in fusion-negative (PFN) tumors (6.4% frequency); no RAS mutations in fusion-positive PAX (PFP) tumors PMID:24436047
  • KRAS focal amplification observed in ESCC tumors PMID:24686850
  • KRAS activating mutations are rare in HCC (~1%; 4.4% of 1,318 ctDNA samples in BEAMing screening); a biomarker-enriched phase II of refametinib + sorafenib in 16 RAS-mutant patients reported median OS 12.7 months. PMID:24798001
  • Mutated in 6% of gastric adenocarcinoma (STAD) overall (TCGA); KRAS/NRAS alterations combined reach 17% across CIN and MSI subtypes PMID:25079317
  • Activating mutations in 33% of LUAD (TCGA, n=230, 74 cancer-associated); mutually exclusive with EGFR; enriched in the transversion-high (TH)/smoker cohort and the PP transcriptional subtype PMID:25079552
  • Driver mutation 100% concordant between primary and metastasis in CRC; established trunk event; mutation status guides cetuximab/panitumumab eligibility and is reliably detected from either tumor site PMID:25164765
  • Hotspot mutations in 5/22 gynaecologic carcinosarcomas (27%); flagged as actionable candidates for MEK/BRAF inhibition PMID:25233892
  • RAS codon 12/61 SSNVs (NRAS/HRAS/KRAS) found in 52/402 (12.9%) papillary thyroid tumors; characterize the follicular variant and drive the RL (RAS-like) phenotype with concurrent MAPK/PI3K signaling; mutually exclusive with BRAFV600E PMID:25417114
  • KRAS activating mutations (G12D, G12V, Q61H) in 24–27% intrahepatic and 37–46% extrahepatic CCA; G12/G13 alterations predict poor prognosis; synergizes with ARID1A loss to drive cholangiocarcinogenesis PMID:25526346
  • KRAS p.G13D mutation present in a distinct subclone in a multi-region WGS case (Pt1) of gastric adenocarcinoma, co-occurring with PIK3CA p.E542K and BRCA2 frameshift across separate clones PMID:25583476
  • KRAS showed significantly higher mutation frequency in African American than Caucasian MSS colorectal cancers (103 AA vs 129 Caucasian), while overall classic CRC driver gene rates (APC, TP53, KRAS, PIK3CA, SMAD4, BRAF, FBXW7) did not differ as a group. PMID:25583493
  • KRAS G12C identified as an activating mutation in metastatic cSCC (n=29); activating oncogene mutations in 11/29 (38%) samples were nearly mutually exclusive. PMID:25589618
  • KRAS cited in the context of murine KRAS/p53 knockout cholangiocarcinoma models that inadequately recapitulate human cholestatic CCA pathophysiology; humanized or organoid systems proposed as alternatives. PMID:25608663
  • KRAS mutated in 7/14 DCB vs 1/17 NDB NSCLC patients treated with pembrolizumab; authors attribute the imbalance to the established smoking–KRAS association rather than a direct causal effect on PD-1 response. PMID:25765070
  • KRAS low-frequency alteration in HCC; part of MAP kinase pathway with low-frequency but FDA-druggable alterations in the 243-case European HCC cohort PMID:25822088
  • KRAS mutated in 92% of pancreatic ductal adenocarcinomas (109-case WES cohort); codon-12 alleles (G12D/G12V/G12C/G12R/G12S) dominate; codon-61 alleles (Q61H/Q61K/Q61R) associated with favourable survival (P=0.01999) and lower pERK staining; mutually exclusive with BRAF and PIK3CA lesions PMID:25855536
  • KRAS rare hot-spot mutations (G12D/G12R/Q61R) in cutaneous melanoma (TCGA 333-sample cohort); mutually exclusive with NRAS and BRAF V600/K601 hot-spots; part of the RAS-mutant melanoma subtype PMID:26091043
  • Significant association with T stage in UTUC; part of the subset of UTUC tumors with FGFR3/HRAS/KRAS mutations associated with lower CNA burden and a ‘low-grade-tumor-progression’ carcinogenesis model PMID:26278805
  • KrasG12D knock-in by AAV-CRISPR HDR in rats yielded ER+/PR+ ductal carcinoma with papillary features at ~70-day median latency; the same edit in mice produced ER-/PR- metaplastic tumors with squamous differentiation, illustrating species-specific lineage plasticity — KRAS is not commonly mutated in human breast cancer PMID:26437033
  • Mutated in n=14 cases as part of the 4.1% RAS-mutant CLL fraction in a 538-sample WES cohort; therapeutic exploration of MAPK-ERK inhibitors is suggested for the RAS/BRAF/MAP2K1-mutant subset PMID:26466571
  • Major activated RAS-pathway oncogene in periampullary adenocarcinoma; RTK/RAS/PI3K pathway activated in 84–94% of cases across three anatomical subtypes (AMPAC, DUOAC, CAC; n=160); KRAS is one of four MutSig-CV-significant genes restricted to the CAC subset PMID:26804919
  • n=25 KRAS mutations in pan-glioma TCGA cohort (n=1122); confirmed as a recurrently mutated Ras-pathway oncogene in human glioma, previously known mainly from engineered mouse models; co-occurs with NRAS (n=5) PMID:26824661
  • KRAS mutations occur collectively with NRAS and HRAS in 28% of PDTC and 24% of ATC; RAS mutations are mutually exclusive with BRAF V600E and gene fusions; RAS-mutant PDTCs trend toward distant metastasis PMID:26878173
  • Known CRC driver identified as a source of recurrent neopeptides; neoantigen load analysis in 619 colorectal cancer cases PMID:27149842
  • Co-occurs with activating PPP3CA mutations (p=0.033) in lung ADC in the TCGA pan-lung cohort; KRAS is a key Ras/Raf/RTK pathway driver considered when calculating the 76% actionable-driver fraction in lung ADC PMID:27158780
  • Classical hotspot activating mutations at codon 12 observed in 11 breast cancer samples; did not meet Mut-driver criteria as a standalone breast-cancer driver event; cited as a cross-cancer driver candidate suggesting drug repurposing potential PMID:27161491
  • KRAS mutations are under-represented in young-onset lung cancer (~9% in <40 yrs vs ~30% in 60-69 yrs); G12C and G12D dominate in the few KRAS-mutant young cases; Indian YLC data (Malik et al., n=133) showed 3.7% KRAS mutation rate PMID:27346245
  • KRAS hotspot mutations in 22/180 patients (12.2%; 23 total mutations, G12 dominant) in advanced germ cell tumors; enriched in seminomas overall (20% vs 8.7% in nonseminoma; P=.045); in nonseminomas, 8 of 11 KRAS mutations occurred in cisplatin-resistant tumors; MEK inhibitors nominated as candidate therapy PMID:27646943
  • KRAS Q61H and G12C activating mutations identified in pediatric ALL and neuroblastoma (NBL) as MEK-inhibitor targets; KRAS V14I also co-occurred with STAT5B I704L and JAK1 K1026E in T-BLL PMID:28007021.
  • KRAS amplified in subsets of esophageal adenocarcinoma (EAC) alongside ERBB2, EGFR, IGF1R, and VEGFA amplifications in a multi-platform genomic characterization of gastroesophageal adenocarcinoma PMID:28052061.
  • 218 patients with KRAS mutations in prospective LUAD cohort (860 patients, MSK-IMPACT); codon 12 dominant; codon 61 in 12/235 (5%) of KRAS-mutated tumors; only 0.9% (2/218) received matched therapy; mutually exclusive with EGFR (p<0.0001) PMID:28336552
  • Single-patient missense event in acral lentiginous melanoma (ALM) integrated genomic study (34 patients) PMID:28373299
  • 6/23 (26%) endometrial polyps harbored low-VAF KRAS hotspot mutations including G12V and G13V; one sample bore both on independent reads; may indicate precursor lesion biology PMID:28445112
  • Driver SNVs targeted in LUAD ctDNA panels; KRAS amplification (>15 copies) identified as an ancestral subclonal event driving lymph-node residual disease in patient CRUK0013 that responded to adjuvant chemoradiotherapy; SNV status not associated with pre-operative ctDNA detection rate within LUADs PMID:28445469
  • Q61H missense mutation in 1/19 sequenced 1p/19q-codeleted oligodendroglioma cases; OncoKB Level 3B PMID:28472509
  • Second most altered gene in a 62-tumor-type pan-cancer cohort (15% overall); G12 codon dominates (80% of KRAS mutations); 90% mutation rate in PAAD, 44% in COAD; limited clinical actionability noted with then-available drugs PMID:28481359
  • Assessed in the 7-gene cross-histology panel for clear-cell endometrial carcinoma; mutations enriched in endometrioid-like (UEC) molecular profile subgroup PMID:28485815
  • Mutations significantly more frequent in intrahepatic cholangiocarcinomas vs. other CCA subtypes (q < 0.1) PMID:28667006
  • Altered in 51/500 (10.2%) of metastatic solid tumors in a pan-cancer metastatic sequencing cohort (MET500) PMID:28783718
  • Hotspot MAPK-pathway mutations in ~5% of prostate cancer patients across disease states PMID:28825054
  • Recurrently focally amplified SCNA in MIBC (n=412, TCGA BLCA 2017). PMID:28988769
  • Oncogenic alterations in 16% of CIN gastroesophageal cancer tumors; acquired activating co-mutations enriched post-trastuzumab progression (2% pre vs 13% post; associated with intrinsic and acquired trastuzumab resistance). PMID:29122777
  • Mutated in 44% of MSS metastatic CRC; hotspot mutations are OncoKB Level 1 resistance markers for anti-EGFR antibodies; enriched in right-sided primaries; HR=1.40 for OS in multivariate analysis PMID:29316426
  • Mutated in 83 NSCLC patients (34%); KRAS mutation alone did not stratify durable clinical benefit to anti-PD-(L)1 therapy; DCB rate 36%, comparable to overall cohort PMID:29337640
  • Cited as a comparator oncogenic driver with approved targeted therapies achieving higher response rates than neratinib in HER2-mutant disease; not a qualifying alteration in the SUMMIT basket trial PMID:29420467
  • Referenced from prior targeted-panel literature as a recurrent alteration in HPV(−) vulvar SCC; not specifically identified as a new finding in this WES cohort (N=15) PMID:29422544
  • KRAS established hotspot mutations newly reach statistical significance (SMG status) in prostate cancer in the 1,013-sample WES meta-cohort (prad_p1000); RAS/RAF/MAPK pathway altered in 5% of PRAD overall. PMID:29610475

Cancer types (linked)

  • LUAD — KRAS G12C enrichment in liver-metastasizing primaries and truncal KRAS in brain-metastatic trajectories PMID:37084736 PMID:37591896.
  • APAD — RAS-mut predominant MAAP subtype has best prognosis and 50% first-line chemotherapy response PMID:36493333.
  • LCH / ECD — KRAS mutated in 7% of histiocytosis PMID:36862133.
  • Advanced NSCLC — ctDNA-detected KRAS associated with worse prognosis PMID:36357680.
  • PAAD — KRAS altered in 90% of resected PDAC; G12R is prognostically favorable (early-stage, node-negative, longer OS) while G12D drives canonical KRAS/EMT programs PMID:39214094.
  • CESC — mutations in 12%, enriched in gastric-type (27%) and UEA (20%); G12C inhibitors considered actionable PMID:37643132.
  • RMS — RAS pathway driver in FN-RMS PMID:37730754.
  • HCC — cfDNA-exclusive alteration (OncoKB level 4) in one of 37 paired samples PMID:37769223.
  • EGC (esophagogastric) — resistance mechanism and inferior PFS association in HER2-positive EGC receiving pembrolizumab + trastuzumab + chemotherapy PMID:37406106.
  • UCEC — 21% in White, 12% in Black EC patients; linked to endometrioid histology prevalence PMID:37651310.
  • PAAD (MSK 2,336-patient cohort) — KRAS-mutant 95%; mutant-allele dosage gains prognostic across all stages; G12R independently better OS vs G12D; approximately 10% of patients have OncoKB level 1–2 biomarkers and an additional 78% level 3A (G12D/V/R/A/S) based on the RAS-inhibitor pipeline. PMID:39753968
  • BLCA — KRAS detected in cfDNA from metastatic urothelial carcinoma; ctDNA frequency numerically higher than matched tumor. PMID:40256659

Co-occurrence and mutual exclusivity

Therapeutic relevance

  • ctDNA-guided matching to targeted therapy in NSCLC (including KRAS-directed regimens) yielded OS benefit vs untreated ctDNA-positive patients (HR 0.63, 95% CI 0.52–0.76, P<0.001) PMID:36357680.
  • RAS-mut predominant MAAP shows 50% first-line chemotherapy response vs 6% in GNAS-mut predominant MAAP (P=.03) PMID:36493333.

Open questions

  • Mechanistic basis for apparent loss of KRAS G12C clones in matched liver metastases of LUAD is unresolved PMID:37084736.
  • Mechanistic basis for reduced metastatic propensity of KRASG12R PAAD beyond the NF-κB / EMT axis identified by spatial profiling and organoids remains to be resolved PMID:39214094.
  • Whether KRAS mutations in dMMR gynecologic cancers are bystander events (passenger due to MSI) or functional drivers of immune evasion requires investigation PMID:38653864.
  • The VTE risk associated with KRAS ctDNA detection appears independent of specific genomic content by multivariate analysis, suggesting a general cancer burden signal rather than KRAS-specific thrombogenicity PMID:39147831.
  • How KRAS mutant-allele dosage gains in PDAC modify response to novel pan-RAS / KRAS-allele-specific inhibitors (e.g., RMC-6236) is unknown; clinical-trial cohorts stratified by dosage are needed. PMID:39753968
  • Whether the ctDNA-detected KRAS in metastatic urothelial carcinoma (CALGB 90601) represents tumor shedding rather than a specific clonal driver event in that cancer type requires further investigation. PMID:40256659

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