ReviewCurrent oncology reports2023
Resistance to KRAS G12C Inhibition in Non-small Cell Lung Cancer.
Review in Current oncology reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 2 of them syntheses that pooled it.
What it found
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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
27 citing papers in PubMed, 2 syntheses or guidelines pooled it, 35 citations in OpenAlex.
- KEAP1 mutations as key crucial prognostic biomarkers for resistance to KRAS-G12C inhibitors.Journal of translational medicine · 2025Pooled it
- Current status of KRAS G12C inhibitors in NSCLC and the potential for combination with anti-PD-(L)1 therapy: a systematic review.Frontiers in immunology · 2025Pooled it
- The CRABP2-MDK Signaling Axis Promotes Lung Adenocarcinoma (LUAD) Progression and Highlights Prognostic Biomarkers.Molecular carcinogenesis · 2026Article
- Review
- Precision Therapeutics in Pancreatic Cancer: Emerging Targeted, Immune, and Antibody-Drug Conjugate Strategies Exemplified by Adagrasib, Dostarlimab, and Trastuzumab Deruxtecan.Journal of clinical medicine · 2026Review
- Evolution from KRAS G12C-mutant to ALK fusion-positive stage IV lung adenocarcinoma following immune checkpoint inhibitor therapy: a case report.Frontiers in oncology · 2026Article
- Role of signaling pathways in lung cancer development and advances in targeted therapies (Review).Oncology letters · 2025Review
- Drug resistance in cancer: molecular mechanisms and emerging treatment strategies.Molecular biomedicine · 2025Review
- Kirsten rat sarcoma G12C inhibitor treatment for a patient with relapsed metastatic lung adenocarcinoma: A case report.World journal of clinical cases · 2025Article
- Advances in biomarkers of resistance to KRAS mutation-targeted inhibitors.Discover oncology · 2025Review
- KRAS G12C Inhibition in Solid Tumors: Biological Breakthroughs, Clinical Evidence, and Open Challenges.Cancers · 2025Review
- Chaperone directed heterobifunctional molecules circumvent KRASCancer letters · 2025Article
- The complex journey of targeting RAS in oncology.BMC cancer · 2025Review
- Progress of KRAS G12C inhibitors in the treatment of refractory colorectal cancer and strategies for drug resistance response.Investigational new drugs · 2025Review
- KRASG12D drives immunosuppression in lung adenocarcinoma through paracrine signaling.JCI insight · 2025Article
- Analysis of Pan-Specific Inhibitors of Oncogenic Mutant Forms of KRAS GTPase.Current medicinal chemistry · 2025Review
- KRAS-mediated upregulation of CIP2A promotes suppression of PP2A-B56α to initiate pancreatic cancer development.Oncogene · 2024Article
- MYC and KRAS cooperation: from historical challenges to therapeutic opportunities in cancer.Signal transduction and targeted therapy · 2024Review
- KRAS-mediated upregulation of CIP2A promotes suppression of PP2A-B56α to initiate pancreatic cancer development.bioRxiv : the preprint server for biology · 2024Article
- The Triterpenoid CDDO-Methyl Ester Reduces Tumor Burden, Reprograms the Immune Microenvironment, and Protects from Chemotherapy-Induced Toxicity in a Preclinical Mouse Model of Established Lung Cancer.Antioxidants (Basel, Switzerland) · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purpose of reviewAlthough the recent development of direct KRAS RECENT
findingsMechanisms of acquired resistance to G12Ci are heterogenous including both on-target and off-target resistance. On-target acquired resistance includes secondary codon 12 KRAS mutations, but also acquired codon 13 and codon 61 alterations, and mutations at drug binding sites. Off-target acquired resistance can derive from activating mutations in KRAS downstream pathway (e.g., MEK1), acquired oncogenic fusions (EML4-ALK, CCDC176-RET), gene level copy gain (e.g., MET amplification), or oncogenic alterations in other pro-proliferative and antiapoptotic pathways (e.g., FGFR3, PTEN, NRAS). In a fraction of patients, histologic transformation can also contribute to the development of acquire resistance. We provided a comprehensive overview of the mechanisms that limit the efficacy of this G12i and reviewed potential strategies to overcome and possibly delay the development of resistance in patients receiving KRAS directed targeted therapies.
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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.