KRAS

Where the papers sit

45 papers from the last 6 months study KRAS directly · updated from PubMed 11 Oct 2026

• KRAS-Driven Pancreatic Cancer

  Allele-selective KRAS inhibition is moving into pancreatic cancer treatment, while combination strategies aim to deepen regression and delay resistance. Daraxonrasib and RAF/EGFR-directed approaches are paired with metabolic interventions targeting lipophagy-dependent fatty-acid oxidation or methionine dependence. Early transformation studies and ctDNA assays are improving selection and detection beyond tissue NGS. Resistance, pathway reactivation, and translation of organoid findings into durable clinical benefit remain open questions.

  15 papers · 33.3%

• KRAS-Targeted Lung Cancer Therapy

  KRAS blockade in lung adenocarcinoma is being linked to immune activation and differentiation-state vulnerabilities rather than pursued as isolated cytotoxic therapy. G12V degradation can regress tumors, but relapse through dysregulated proteolysis and cellular plasticity exposes limits of single-node targeting. Mutant p53, SPP1, bystander killing, immune-checkpoint blockade, and engineered T-cell or ADC strategies recur as ways to address heterogeneity. Evidence remains mainly preclinical, with the durability and clinical breadth of these combinations unresolved.

  11 papers · 24.4%

• Mutation-Selective KRAS Therapy

  KRAS drug development is expanding beyond direct blockade toward degraders, pan-KRAS inhibitors, G-quadruplex stabilizers, and RNA delivery. G12D and G12V tumors are prominent targets, while AGO2 disruption and predicted synthetic lethal partners seek to widen response and sensitize chemo-immunotherapy. Resistance mapping in colorectal cancer is becoming a central guide for combination design. TP53/KRAS co-mutation and KRAS-associated prognostic studies extend the question from response to patient selection, but durable activity across tumor types remains unsettled.

  10 papers · 22.2%

• Others — Cancer Genomics and Drug Discovery

  NSCLC work centers on matching KRAS genotype and co-mutations to immunotherapy, neoadjuvant treatment, and candidate drugs. STK11 and KEAP1 status, G12C versus non-G12C alleles, and ctDNA detection recur as determinants of prognosis or treatment allocation. Computational repurposing, molecular docking, and phytochemical screens expand the search for anti-KRAS activity, while stress-response biology offers a metastasis mechanism. The cluster also contains unrelated leukemia, protein-evolution, and assay studies, so it does not support one unified therapeutic direction.

  9 papers · 20%