ArticleNPJ precision oncology2025
Molecular characterization and prognostic implications of KRAS mutations in pancreatic cancer patients: insights from multi-cohort analysis.
Article in NPJ precision oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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The trial behind it
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Who cites it
11 citing papers in PubMed.
- ERCC6 at the Transcription-Replication Interface: Integration of Transcription-Coupled Repair with Replication Stress Responses.International journal of molecular sciences · 2026Review
- KRAS signaling networks, mutational heterogeneity, and emerging therapeutic strategies for cancer treatment.Biomarker research · 2026Review
- Review
- The AUTACE That Degrades KRAS and Engages CD8Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Article
- Current advances in immunotherapy for KRAS-Mutant pancreatic cancer.Clinical and experimental medicine · 2026Review
- Peptides as integrative modulators for clinical prognosis and targeted therapy in pancreatic cancer.Discover oncology · 2026Review
- Lateral flow immunochromatographic assay (LFIA) for tumor marker detection: technical evolution, clinical translation challenges, and future perspectives.Mikrochimica acta · 2026Review
- Molecular Profiling and Survival Outcomes in Pancreatic Ductal Adenocarcinoma: A Multicenter Real-World Study from Turkey.Current oncology (Toronto, Ont.) · 2026Article
- Computational identification and mechanistic characterization of natural product binders targeting the PDE6D prenyl binding tunnel.Scientific reports · 2026Article
- KRAS Inhibition in Pancreatic Ductal Adenocarcinoma.Journal of clinical medicine · 2026Review
Corrections and comments
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Authors and funding
15 authors.
Funding
Abstract
KRAS mutations drive pancreatic adenocarcinoma (PDAC) progression. This study investigates molecular heterogeneity among KRAS subtypes and their prognostic implications. This study explores KRAS mutations in PDAC, analyzing molecular heterogeneity and prognosis across our hospital cohort (SDFM, n = 113) with TCGA cohort (n = 183) and QCMG cohort (n = 383). KRAS, TP53, CDKN2A, and SMAD4 were the main mutated genes. Co-mutations of KRAS with TP53, and TP53 with CDKN2A, correlated with higher tumor mutation burden and poorer outcomes. KRAS subtypes G12D and Q16&others had worse prognosis than G12V and G12R. Combining TP53 status with KRAS subtypes improved risk stratification: high-risk patients had shorter survival (P ≤ 0.001), higher PD-L1 expression, P53 pathway alterations, fewer CD4+/CD8 + T cells and macrophages (p < 0.05), but more neutrophils (p < 0.001). These findings underscore the prognostic impact of KRAS and TP53 mutations, guiding personalized treatment.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.