ReviewMolecular cancer2021
Oncogenic KRAS blockade therapy: renewed enthusiasm and persistent challenges.
Review in Molecular cancer, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 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
48 citing papers in PubMed, 74 citations in OpenAlex.
- SNU523 Inhibits Pancreatic Cancer through the Dual Suppression of STAT3 and MEK Signaling Pathways.ACS omega · 2026Article
- Small-molecule RAS/RAF inhibitors target RAS-driven cancers via allosteric RAF disruption.Nature communications · 2026Article
- Targeting macropinocytosis for cancer therapy.Nature reviews. Cancer · 2026Review
- Identification of KRAS mutants (G12C, G12D, and G12V) inhibitors.Future medicinal chemistry · 2025Article
- Differential Response and Resistance to KRAS-Targeted Therapy.Molecular carcinogenesis · 2025Review
- Targeting KRAS Sensitizes Ferroptosis by Coordinately Regulating the TCA Cycle and Nrf2-SLC7A11-GPX4 Signaling in Hepatocellular Carcinoma.Smart medicine · 2025Article
- Study on the Synergistic Effect of Klotho and KRAS on Reducing Ferroptosis After Myocardial Infarction by Regulating RAP1/ERK Signaling Pathway.Applied biochemistry and biotechnology · 2025Article
- The Persistent Power of the Taxane/Platin Chemotherapy.Cancers · 2025Review
- MVASA-HGN: multi-view adaptive semantic-aware heterogeneous graph network forQuantitative imaging in medicine and surgery · 2025Article
- Digestive cancers: mechanisms, therapeutics and management.Signal transduction and targeted therapy · 2025Review
- Review
- Article
- SRC kinase drives multidrug resistance induced by KRAS-G12C inhibition.Science advances · 2024Article
- RAS signaling in carcinogenesis, cancer therapy and resistance mechanisms.Journal of hematology & oncology · 2024Review
- KRAS Mutation Subtypes and Their Association with Other Driver Mutations in Oncogenic Pathways.Cells · 2024Review
- Triple Blockade of Oncogenic RAS Signaling Using KRAS and MEK Inhibitors in Combination with Irradiation in Pancreatic Cancer.International journal of molecular sciences · 2024Article
- Review
- KRAS: Biology, Inhibition, and Mechanisms of Inhibitor Resistance.Current oncology (Toronto, Ont.) · 2024Review
- Farnesyl-transferase inhibitors show synergistic anticancer effects in combination with novel KRAS-G12C inhibitors.British journal of cancer · 2024Article
- NPS-2143 inhibit glioma progression by suppressing autophagy through mediating AKT-mTOR pathway.Journal of cellular and molecular medicine · 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
3 authors at 3 institutions in 3 countries.
Funding
Abstract
Across a broad range of human cancers, gain-of-function mutations in RAS genes (HRAS, NRAS, and KRAS) lead to constitutive activity of oncoproteins responsible for tumorigenesis and cancer progression. The targeting of RAS with drugs is challenging because RAS lacks classic and tractable drug binding sites. Over the past 30 years, this perception has led to the pursuit of indirect routes for targeting RAS expression, processing, upstream regulators, or downstream effectors. After the discovery that the KRAS-G12C variant contains a druggable pocket below the switch-II loop region, it has become possible to design irreversible covalent inhibitors for the variant with improved potency, selectivity and bioavailability. Two such inhibitors, sotorasib (AMG 510) and adagrasib (MRTX849), were recently evaluated in phase I-III trials for the treatment of non-small cell lung cancer with KRAS-G12C mutations, heralding a new era of precision oncology. In this review, we outline the mutations and functions of KRAS in human tumors and then analyze indirect and direct approaches to shut down the oncogenic KRAS network. Specifically, we discuss the mechanistic principles, clinical features, and strategies for overcoming primary or secondary resistance to KRAS-G12C blockade.
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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.