ReviewFrontiers in pharmacology2025
Therapeutic strategies for KRAS G12C-mutant non-small cell lung cancer: from bench to bedside and beyond.
Review in Frontiers in pharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
3 citing papers in PubMed.
- The Role of KRAS in Non-Small Cell Lung Cancer: From Molecular Background to Precision Medicine.International journal of molecular sciences · 2026Review
- Advancing KRAS Modulation: Expanding Chemical Space toward Broad-Spectrum RAS-Driven Oncology.ACS medicinal chemistry letters · 2026Article
- Therapeutic Targeting of VEGFR-2, PD-L1, and EGFR-MET Pathways in Non-Small Cell Lung Cancer: Clinical Progress with Ramucirumab, Atezolizumab, and Amivantamab.Journal of clinical medicine · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
KRAS is one of the most frequently mutated oncogenes in non-small cell lung cancer (NSCLC), particularly in lung adenocarcinoma, with mutation rates ranging from 15% to 25%. Historically considered "undruggable," KRAS has recently become a viable therapeutic target with the development of selective KRAS G12C inhibitors such as sotorasib (AMG510) and adagrasib (MRTX849). These inhibitors have demonstrated promising clinical efficacy; however, their effectiveness is frequently limited by the emergence of resistance mechanisms. This review provides a comprehensive analysis of KRAS G12C structural biology, its role in oncogenic signaling, and the challenges associated with targeted therapy. We discuss the mechanisms of intrinsic and acquired resistance, current monotherapy limitations, and the rationale for combination strategies aimed at overcoming resistance. Additionally, we explore future therapeutic perspectives, including novel inhibitors, combination regimens, and emerging precision medicine approaches, to optimize treatment outcomes for patients with KRAS G12C-mutant NSCLC.
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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.