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Radiomics and Machine Learning in Medical Imaging / Lung Cancer Treatments and Mutations · Journal article
Cancer Research Communications · August 11, 2026
Encouraging direction, but not yet definitive.
This single-arm neoadjuvant study of 13 EGFR-mutant NSCLC patients receiving short-term gefitinib (median 1.4 months) reports objective response in 62% and pathological downstaging in 46%, coupled with detailed genomic and transcriptomic remodelling without common resistance mutations. The findings are mechanistically interesting and suggest early therapeutic vulnerabilities, but lack a concurrent control arm and rely on surrogate molecular endpoints rather than progression-free or overall survival outcomes.
Single-arm prospective neoadjuvant cohort study with multi-region and spatial molecular profiling. Patients with stage IA–IIIA EGFR-mutated NSCLC undergoing neoadjuvant therapy followed by surgery.. Intervention: Neoadjuvant gefitinib 250 mg daily. Compared with: Purity-matched treatment-naïve tumour cohort (not concurrent). n = 13. Not specified in abstract.
Objective response rate 62% (8 of 13 patients); disease control rate 100% on neoadjuvant gefitinib Pathological downstaging occurred in 46% of patients; major pathological response in 8% On-treatment tumours showed reduced tumour purity, decreased EGFR amplification, and increased immune regulatory/inflammatory gene expression compared with treatment-naïve tumours
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The molecular signatures of early EGFR inhibition response may identify rational combination therapy targets; however, the small single-arm design and lack of clinical outcome data (PFS, OS) limit immediate clinical translation. Results warrant confirmation in a randomised controlled trial with hard clinical endpoints.
Single-arm neoadjuvant study with comprehensive molecular profiling showing early tumour and microenvironmental changes, but limited by small sample size, lack of control arm, and surrogate endpoints rather than hard clinical outcomes.
As stated by the source record.
Quoted from the source exactly as published.
The molecular signatures of early EGFR inhibition response may identify rational combination therapy targets; however, the small single-arm design and lack of clinical outcome data (PFS, OS) limit immediate clinical translation. Results warrant confirmation in a randomised controlled trial with hard clinical endpoints.
Graded across the dimensions that decide whether you should act, each from what the source actually supports. There is no single score, and where a dimension was not assessed it says so.
Abstract Purpose: Despite widespread use of targeted therapies, little is known about how tumours and their microenvironment respond in the earliest phases of treatment, and whether these early changes reveal new therapeutic opportunities. In this study, we investigated how short-term EGFR inhibition reshapes tumour biology and the tumour microenvironment using comprehensive multi-region and spatial molecular profiling. Patients and Methods: Patients with stage IA–IIIA EGFR mutated NSCLC received at least 4 weeks of gefitinib (250 mg daily) before surgery. Multi-region whole-exome and RNA sequencing of resected tumours were compared with a purity-matched treatment-naïve cohort. Results: Thirteen patients received neoadjuvant gefitinib for a median of 1.4 months, achieving objective response and disease control rates of 62% and 100%, respectively. Pathological downstaging occurred in 46% of patients, with major pathological response in 8%. Deep genomic and transcriptomic profiling revealed rapid tumour and microenvironmental adaptation to EGFR inhibition without emergence of common acquired resistance mutations such as EGFR T790M. Compared with treatment-naïve tumours, on-treatment tumours showed reduced tumour purity, decreased EGFR amplification, increased immune regulatory and inflammatory gene expression, and a metabolic shift from glycolysis to oxidative phosphorylation, spatially validated. Conclusions: These findings show that early EGFR inhibition triggers coordinated remodelling of tumour cells and the microenvironment, uncovering new therapeutic vulnerabilities and opening a window for rational combination strategies to improve outcomes in EGFR mutated NSCLC.
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