ReviewCancers2025
KRAS G12C Inhibition in Solid Tumors: Biological Breakthroughs, Clinical Evidence, and Open Challenges.
Review in Cancers, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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
5 citing papers in PubMed.
- Review
- Thermal Stability, Plasma Pharmacokinetics, and Tumor Response Modeling of a Cell-Penetrating Protein That Cleaves RAS Family GTPases.ACS pharmacology & translational science · 2026Article
- Oncogene-Mechanics Axis: KRAS G12C Confers Agility Enabling Malignant Mechano-responses to Peristalsis in Colorectal Cancer.bioRxiv : the preprint server for biology · 2026Article
- Cancer Drug Development in Never-Smoker Lung Cancer: Targeted and Immune-Based Therapeutic Strategies.Oncology research · 2026Review
- Targeted therapy for KRAS G12C-mutated colorectal cancer: advances, challenges, and future directions.American journal of cancer research · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
KRAS is the most frequently mutated oncogene in cancer. Its activating mutations are associated with aggressive tumor behavior and resistance to certain therapies, including anti-EGFR treatments in colorectal cancer. In particular, the KRAS G12C mutation, which accounts for approximately 3-4% of colorectal cancers (CRCs) and 12-14% of non-small cell lung cancers (NSCLCs), involves a cysteine substitution at codon 12. This has provided the opportunity to develop selective covalent inhibitors that trap the mutant protein in its inactive state. The first targeted therapies for KRAS G12C-mutant cancers comprise sotorasib and adagrasib, both of which have been authorized for use in patients with previously treated NSCLC and CRC. Nevertheless, despite the evidence of clinical activity for this class of agents, primary and acquired resistance, dose optimization, and toxicity management remain significant open challenges. In this review, we summarize recent advances in KRASG12C tumor biology and pharmacological targeting. We also provide additional insights to guide future efforts to overcome the limitations of the current approaches and implement the treatment of KRASG12C-mutant cancers.
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Identifiers
What OpenQuestion holds
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.