EGFR mutation

P3, N=390, Active, not recruiting, National Cancer Institute (NCI) | Trial completion date: Oct 2026 --> Feb 2027 | Trial primary completion date: Oct 2026 --> Dec 2025

P2, N=16, Not yet recruiting, Jonsson Comprehensive Cancer Center | Trial completion date: Dec 2029 --> Jun 2030 | Initiation date: Jan 2026 --> Jun 2027 | Trial primary completion date: Dec 2028 --> Jun 2029

P1, N=16, Terminated, Rutgers, The State University of New Jersey | Active, not recruiting --> Terminated; accrual goal met

P1/2, N=24, Not yet recruiting, University of Chicago

Importantly, we identify resistance mechanisms specific to protein degraders: E3 ligase loss or mutation, EGFR alterations that disrupt ternary complex formation, deubiquitinase upregulation, and degradation pathway dysfunction. By integrating structural biology, medicinal chemistry, and clinical insights, this review provides a comprehensive roadmap for developing next-generation EGFR degraders capable of overcoming resistance and improving outcomes for lung cancer patients.

EGFR mutation discordance is common and clinically relevant, particularly in NSCLC, but varies substantially by sampling strategy, biofluid, treatment context, and metastatic site. Given the high between-study heterogeneity and the predominance of NSCLC and Asian cohorts, pooled estimates should be interpreted as descriptive summaries rather than universally generalisable benchmarks. These findings support integrated and context-aware sampling strategies for EGFR-targeted therapy and resistance monitoring.

TP53 and EGFR gene mutations were associated with more aggressive cancer phenotypes, leading to a 2.6-fold increase in the risk of death.

P1/2, N=31, Active, not recruiting, Washington University School of Medicine | N=114 --> 31 | Recruiting --> Active, not recruiting

Compared to results from established architectures such as Inception-v3 on the same WSIs, our model demonstrated significantly improved performance for most features. With further optimization, our model could support triaging for molecular testing and inform precision treatment strategies for NS-LUAD patients.

Molecular docking and dynamics simulations indicated stable, favorable binding within the ATP-binding sites of both kinases. Collectively, these findings identify compound (11a) as a promising dual-target anticancer lead warranting further preclinical investigation.

P1, N=21, Recruiting, Marcela V. Maus, M.D.,Ph.D. | Trial primary completion date: Jun 2026 --> Sep 2026 | Trial completion date: Jun 2027 --> Sep 2027