EGFR amplification

P2, N=78, Recruiting, L. Nicolas Gonzalez Castro, MD, PhD | Trial completion date: Nov 2026 --> Mar 2027 | Trial primary completion date: Feb 2026 --> Aug 2026

The tumor habitat imaging model based on advanced MRI was useful for accurately predicting TERT promoter mutation and EGFR amplification status in IDH wild-type glioblastoma.

P2, N=37, Active, not recruiting, National Cancer Institute (NCI) | Trial completion date: May 2026 --> Dec 2026 | Trial primary completion date: May 2026 --> Dec 2026

Our study demonstrated that baseline EGFR amplification defines a clinically distinct, aggressive subtype of treatment-naïve patients with concurrent EGFR L858R mutation and EGFR amplification. Second-generation TKIs showed superior efficacy over third-generation TKIs in this specific population. These findings refine prognostic stratification and support biomarker-guided first-line therapy selection for EGFR L858R-mutant NSCLC with co-occurring EGFR amplification.

Metabolic subtyping identifies DEMs as critical drivers of glioma progression. The DEM-derived risk model, combined with EGFR/IDH status, provides a clinically actionable tool for prognosis and targeted therapy development.

This study represents the largest genomic cohort to date of FGFR alterations in GBM, IDH-wt. FGFR::TACC fusion-positive and FGFR1 mutation-positive GBMs exhibited distinct genetic profiles, highlighting the clinical relevance of molecular subclassification and providing insight for future therapeutic strategies.

IDH mutant gliomas and IDHwt GBM express different progenitor cell markers. THY1 is highly expressed in IDH mutant gliomas.

Disruption of glycosylation at N361, located near the ligand binding and dimerization regions, created a dominant negative form of EGFR, which non-productively co-localized with HER2, resulting in a blockage in proliferation. These findings underline the critical relevance of post-translational glycosylation modifications on EGFR function.

P1, N=56, Active, not recruiting, Mayo Clinic | Recruiting --> Active, not recruiting

In this discourse, we delineate the case of a 42-year-old male patient diagnosed with IDH-wild-type, MGMT-unmethylated, TERT promoter-mutated, and EGFR-amplified GBM, who manifested an early recurrence during adjuvant temozolomide therapy. Our findings, contextualized within contemporary evidence on re-irradiation (stereotactic radiosurgery/fractionated stereotactic radiation therapy) and combinatorial strategies (BEV with lomustine or irinotecan), underscore the need for further empirical investigation to optimize treatment sequencing in r-GBM. This case emphasizes the necessity for individualized multimodal approaches to improve outcomes in this refractory patient population.

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