ArticleScience advances2025
Steric disruption of EGFR oligomerization overcomes therapy resistance in non-small cell lung cancer.
Article in Science advances, 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.
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
2 citing papers in PubMed.
- Optimization of ultrasound-assisted extraction of Sargassum polycystum for antitumor activity: Multi-objective optimization and mechanistic insights.Ultrasonics sonochemistry · 2026Article
- MicroRNA-regulated signaling and tumor microenvironment modulation in lung cancer: mechanistic insights and translational opportunities.Cancer cell international · 2026Review
Corrections and comments
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Authors and funding
4 authors.
Funding
Abstract
Acquired drug resistance mutations in epidermal growth factor receptor (EGFR) present a substantial clinical challenge in treating non-small cell lung cancer (NSCLC). While EGFR oligomerization plays a pivotal role in modulating receptor signaling, its relationship with resistance mutations remains unclear. Here, we investigated the real-time link between oligomerization of oncogenic and resistant EGFR mutants and downstream signaling using a fluorescent protein-based proximity probe and signaling reporter in living cells. We found that EGFR mutants resistant to tyrosine kinase inhibitors (TKIs) exhibited higher oligomerization than did wild-type EGFR with or without EGF. The efficacy of TKIs and allosteric drugs inversely correlated with receptor oligomerization. Furthermore, sterically disrupting EGFR oligomerization by genetically fusing a bulky protein to resistant mutants overcame resistance and suppressed proliferation. Moreover, extracellular application of bulky EGFR binders suppressed resistant mutants by disrupting oligomerization. These findings highlight steric disruption of EGFR oligomerization as a promising strategy for overcoming therapy resistance in NSCLC and introduce a versatile screening platform for developing competitive and allosteric inhibitors.
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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.