ArticleClinical cancer research : an official journal of the American Association for Cancer Research2025
Distinct Molecular and Clinical Features of Specific Variants of KRAS Codon 12 in Pancreatic Adenocarcinoma.
Article in Clinical cancer research : an official journal of the American Association for Cancer Research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.
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Who cites it
18 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Efficacy and toxicities of modified FOLFIRINOX versus gemcitabine plus nab-paclitaxel as first-line chemotherapy for unresectable pancreatic cancer: a systematic review and meta-analysis.Frontiers in oncology · 2026Pooled it
- Current landscape of RAS-targeted therapy for pancreatic cancer.The oncologist · 2026Review
- ARNTL2 promotes metastatic phenotypes through SERPINE1 transcription in KRAS G12D pancreatic cancer.iScience · 2026Article
- Precision immunotherapy in metastatic pancreatic cancer: OPTIMIZE-1 biomarker-driven patient stratification for future studies.Annals of pancreatic cancer · 2026Article
- Pancreatic cancer.Nature reviews. Disease primers · 2026Review
- Crosstalk between KRAS and miRNAs in pancreatic cancer: Opportunities for its diagnosis, prognosis and therapeutic intervention (Review).International journal of oncology · 2026Review
- Deciphering RTK-RAS and MAPK Pathway Dependencies in Gemcitabine-Treated Pancreatic Ductal Adenocarcinoma Through Conversational Artificial Intelligence.International journal of molecular sciences · 2026Article
- Conversational Artificial Intelligence Agents-Enabled Dissection of RTK-RAS and MAPK Pathway Dependencies in Gemcitabine-Treated Pancreatic Ductal Adenocarcinoma (PDAC).medRxiv : the preprint server for health sciences · 2026Article
- Prognostic Implications of Codon-SpecificJCO precision oncology · 2026Article
- KRAS Inhibition in Pancreatic Ductal Adenocarcinoma.Journal of clinical medicine · 2026Review
- Targeting PAK4 promotes Gemcitabine-induced pyroptosis in pancreatic cancer via NLRP1/caspase-3/GSDME axis.Communications biology · 2026Article
- KRAS-driven cytokine-metabolic crosstalk shapes immune exclusion in pancreatic ductal adenocarcinoma.Frontiers in genetics · 2026Review
- KRAS mutations as architects of the tumor immune microenvironment: implications for combination therapies.Frontiers in oncology · 2026Review
- Key Considerations for TargetingDrug design, development and therapy · 2026Review
- Lymph node-targeted, mKRAS-specific amphiphile vaccine in pancreatic and colorectal cancer: phase 1 AMPLIFY-201 trial final results.Nature medicine · 2025Article
- PLK1 inhibition enhances gemcitabine-induced apoptosis through PLK1-dependent ERK1/2-Bim and AKT1/Noxa signals in pancreatic cancer cells.Medical oncology (Northwood, London, England) · 2025Article
- Multi-omics integration and machine learning uncover molecular basal-like subtype of pancreatic cancer and implicate A2ML1 in promoting tumor epithelial-mesenchymal transition.Journal of translational medicine · 2025Article
- Enhancing Early Detection of Pancreatic Cancer in Genetically Predisposed Individuals: Integrating Advanced Imaging Modalities with Emerging Biomarkers and Liquid Biopsy.Biologics : targets & therapy · 2025Review
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16 authors.
Funding
Abstract
purposeOncogenic mutations in KRAS have been identified in >85% of pancreatic ductal adenocarcinoma (PDAC) cases, with G12D, G12V, and G12R being the most frequent variants. Using large clinical and genomic databases, this study characterizes prognostic and molecular differences between KRAS variants, focusing on KRASG12D and KRASG12R. EXPERIMENTAL
designPDAC samples were tested using DNA and RNA sequencing. The MAPK activation score and tumor microenvironment were analyzed from RNA expression data. Real-world overall survival (OS) obtained from insurance claims data was calculated from tissue collection to last contact. Significance was determined by χ2 and Fisher exact tests.
resultsA total of 3,755 patients with PDAC harboring KRASG12D (n = 1,766), KRASG12V (n = 1,294), KRASG12R (n = 621), or KRASG12C (n = 74) variants were identified. Patients with G12R mutations had longer OS compared with those with G12D overall (12.7 vs. 10.1 months; P value = 0.0001), with similar trends in patients treated with gemcitabine/nab-paclitaxel (13.5 vs. 10.4 months; P value = 0.0002) or FOLFIRINOX (18.3 vs. 14.0 months; P value<0.001). ARID1A and KMT2D mutations were more frequent in the G12D subgroup. Several genes involved in glucose and glutamine metabolism were less expressed in G12R compared with G12D. PD-L1 expression was lower in G12R compared with G12D (13% vs. 19%).
conclusionsKRAS G12D tumors exhibited a distinct molecular profile compared with G12R tumors, including genes involved in the MAPK pathway, immune activation, and glucose and glutamine metabolism. Patients with G12D mutations had lower OS compared with those with G12R. Based on these data, future studies should address the KRAS mutation status and explore distinct therapeutic vulnerabilities.
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