ArticleMolecular therapy : the journal of the American Society of Gene Therapy2024
CRISPR-mediated ablation of TP53 and EGFR mutations enhances gefitinib sensitivity and anti-tumor efficacy in lung cancer.
Article in Molecular therapy : the journal of the American Society of Gene Therapy, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Patient-Derived Organoid-Based CRISPR Screens in Cancer Research: Applications, Advances, and Challenges.Cancer medicine · 2026Review
- CRISPR Technology: Transforming the Future of Medicine and Diagnostics.Biochemistry · 2025Review
- Gene editing in cancer therapy: overcoming drug resistance and enhancing precision medicine.Cancer gene therapy · 2025Review
- Review
- A base editing platform for the correction of cancer driver mutations unmasks conserved p53 transcription programs.Genome biology · 2025Article
- Discovery of Drugs Targeting Mutant p53 and Progress in Nano-Enabled Therapeutic Strategy for p53-Mutated Cancers.Biomolecules · 2025Review
- Restoration of TP53 strategy via specific nanoparticles for ovarian cancer therapy.Journal of ovarian research · 2025Article
- An integrative analysis reveals cancer risk associated with artificial sweeteners.Journal of translational medicine · 2025Article
- Coupling enzymatic digestion with nanopore sensing for low-abundance EGFR-L858R mutation detection.Frontiers in bioengineering and biotechnology · 2025Article
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Authors and funding
6 authors.
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Abstract
Multiple pathogenic single-nucleotide polymorphisms (SNPs) have been identified as contributing factors in the aggravation of cancer prognosis and emergence of drug resistance in various cancers. Here, we targeted mutated EGFR and TP53 oncogenes harboring single-nucleotide missense mutations (EGFR-T790M and TP53-R273H) that are associated with gefitinib resistance. Co-delivery of adenine base editor (ABE) and EGFR- and TP53-SNP specific single-guide RNA via adenovirus (Ad) resulted in precise correction of the oncogenic mutations with high accuracy and efficiency in vitro and in vivo. Importantly, compared with a control group treated only with gefitinib, an EGFR inhibitor, co-treatment with Ad/ABE targeting SNPs in TP53 and EGFR in combination with gefitinib increased drug sensitivity and suppressed abnormal tumor growth more efficiently. Taken together, these results indicate that ABE-mediated correction of dual oncogenic SNPs can be an effective strategy for the treatment of drug-resistant cancers.
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