ArticleExperimental & molecular medicine2025
Longitudinal pharmacogenomic analysis of refractory lung cancer to identify therapeutic candidates for epidermal growth factor receptor-tyrosine kinase inhibitor resistance subclones.
Article in Experimental & molecular medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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.
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Who cites it
2 citing papers in PubMed.
- Tumor evolution: signaling pathways, molecular mechanisms and therapeutic targets.Signal transduction and targeted therapy · 2026Review
- Pharmacogenomics in oncology: mutation-targeted therapy and biomarker integration in non-small cell lung cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026Review
Corrections and comments
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Authors and funding
10 authors.
Funding
Abstract
The dynamic nature of longitudinal tumor evolution across patients presents challenges in designing effective drugs. Here we aimed to determine tumor evolution resistance mechanisms and explore candidate drugs for specific tumor evolution types. We conducted longitudinal pharmacogenomic analysis of datasets of 73 samples in 34 patients among a National Cancer Center refractory lung cancer cohort (n = 199). Genomic profiles were determined to identify evolutionary trees in each patient, which were classified into tumor evolution groups according to the predominant truncal mutations, TP53 and epidermal growth factor receptor. These groups were categorized into persistence, extinction and expansion groups according to the status of these two clones. Pharmacogenomic profile analysis identified that XAV-939 was effective for the epidermal growth factor receptor-extinction group exhibiting epithelial-to-mesenchymal transition-activated resistance. In addition, MYC
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