ArticleNPJ precision oncology2023
Evolution of acquired resistance in a ROS1
Article in NPJ precision oncology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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.
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Who cites it
6 citing papers in PubMed, 15 citations in OpenAlex.
- Antitumor Activity of USP7 Inhibitor GNE-6776 in Non-Small Cell Lung Cancer Involves Regulation of Epithelial-Mesenchymal Transition, Cell Cycle, Wnt/β-Catenin, and PI3K/AKT/mTOR Pathways.Pharmaceuticals (Basel, Switzerland) · 2025Article
- Evolutionary rescue model informs strategies for driving cancer cell populations to extinction.bioRxiv : the preprint server for biology · 2025Article
- Cross-attention enables deep learning on limited omics-imaging-clinical data of 130 lung cancer patients.Cell reports methods · 2024Article
- Genomic Landscape of NSCLC in the Republic of Ireland.JTO clinical and research reports · 2024Article
- Insights into direct KRAS inhibition strategies for cancer treatment.Future medicinal chemistry · 2024Review
- Screening biomarkers for predicting the efficacy of immunotherapy in patients with PD-L1 overexpression.Journal of cancer research and clinical oncology · 2023Article
Corrections and comments
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Authors and funding
13 authors at 1 institution in 1 country.
Funding
Abstract
Patients with metastatic NSCLC bearing a ROS1 gene fusion usually experience prolonged disease control with ROS1-targeting tyrosine kinase inhibitors (TKI), but significant clinical heterogeneity exists in part due to the presence of co-occurring genomic alterations. Here, we report on a patient with metastatic NSCLC with a concurrent ROS1 fusion and KRAS p.G12C mutation at diagnosis who experienced a short duration of disease control on entrectinib, a ROS1 TKI. At progression, the patient continued entrectinib and started sotorasib, a small molecule inhibitor of KRAS p.G12C. A patient-derived cell line generated at progression on entrectinib demonstrated improved TKI responsiveness when treated with entrectinib and sotorasib. Cell-line growth dependence on both ROS1 and KRAS p.G12C was further reflected in the distinct downstream signaling pathways activated by each driver. Clinical benefit was not observed with combined therapy of entrectinib and sotorasib possibly related to an evolving KRAS p.G12C amplification identified on repeated molecular testing. This case supports the need for broad molecular profiling in patients with metastatic NSCLC for potential therapeutic and prognostic information.
Identifiers
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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.