ReviewAmerican journal of cancer research2024
The role of m6A methylation in targeted therapy resistance in lung cancer.
Review in American journal of cancer research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Three-year adjuvant treatment of icotinib in stage II-IIIA EGFR-mutated lung adenocarcinoma (ICWIP): a randomized, double-blind, placebo-controlled phase 3 trial.Signal transduction and targeted therapy · 2026Trial
- Reprogramming resistance in advanced lung cancer: epigenetic modulation to restore therapeutic vulnerability.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026Review
- NNature reviews. Cancer · 2026Review
- Research progress on the characteristics and functions of m6A modification in lung cancer tumor stem cells.American journal of cancer research · 2026Review
- Drug resistance in cancer: molecular mechanisms and emerging treatment strategies.Molecular biomedicine · 2025Review
- Emerging Concepts in Immuno-Oncology: Insights from Natural Language Processing-Driven Co-Occurrence Analysis.ACS omega · 2025Review
- RNA Modification in Metabolism.MedComm · 2025Review
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Authors and funding
7 authors.
Funding
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Abstract
Targeted therapies have greatly improved clinical outcomes for patients with lung cancer (LC), but acquired drug resistance and disease relapse inevitably occur. Increasingly, the role of epigenetic mechanisms in driving acquired drug resistance is appreciated. In particular, N6-methyladenosine (m6A), one of the most prevalent RNA modifications, has several roles regulating RNA stability, splicing, transcription, translation, and destruction. Numerous studies have demonstrated that m6A RNA methylation can modulate the growth and invasion of cancer cells as well as contribute to targeted therapy resistance in LC. In this study, we outline what is known regarding the function of m6A in the acquisition of targeted therapy resistance in LC.
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