EGFR mutation

Furthermore, these migratory phenotypes can be rescued with B56α overexpression. Together, these findings implicate B56α as a key regulator of cellular plasticity and highlight the dynamic nature by which PP2A-B56α posttranslationally regulates NSCLC EMT.

This case is the first to elucidate the putative resistance mechanisms to zongertinib in HER2-mutant lung adenocarcinoma might be transformation of adenosquamous with giant-cell carcinoma and acquired HER2 amplification through integrated histological and molecular analyses. These findings highlight the necessity of post-progression biopsy and genomic profiling to characterize resistance evolution and guide subsequent therapy selection.

Background Resistance to targeted cancer therapies, such as osimertinib in EGFR-mutant lung cancer, remains a major obstacle to effective treatment...While performance may vary in cancer types with limited data and potential off-target effects warrant further validation, MMDGNN provides a promising computational foundation for precision oncology. The framework can be extended to broader biomedical applications requiring multimodal molecular inference.

Initial thoracic radiotherapy (50 Gy in 25 fractions) successfully alleviated the SVCS, enabling subsequent systemic therapy with tislelizumab, nab-paclitaxel, and carboplatin...Treatment with a third-generation EGFR-TKI (aumolertinib) was initiated, resulting in significant symptomatic improvement and a progression-free survival of four months...To our knowledge, this is the first report demonstrating the successful sequential integration of radiotherapy and EGFR-TKI therapy in SMARCA4-dNSCLC. Our experience demonstrates that a proactive, individualized multimodal strategy-integrating radiotherapy for local control and targeted therapy guided by dynamic molecular profiling-can significantly extend survival beyond the historical median of approximately 12 months for SMARCA4-deficient NSCLC.

Using the IsoTar target prediction tool, we identified STAT3 as a key regulator and confirmed STAT3 protein downregulation upon transfection with miR-411ed. We further investigated the effect of miR-411ed in vivo, observing a reduction in tumor size with miR-411ed in combination with Osimertinib but not with miR-411ed or Osimertinib treatment alone, confirming the effectiveness of miR-411ed in TKI response.

Tumor burden may serve as a prognostic biomarker in advanced NSCLC receiving EGFR-TKIs. These findings raise the hypothesis that durable survival in low-burden patients may be achievable with monotherapy, potentially sparing unnecessary toxicity from combination regimens. This warrants prospective validation comparing monotherapy versus combination strategies.

P1, N=9, Enrolling by invitation, Beijing Neurosurgical Institute

P3, N=312, Recruiting, Instituto Nacional de Cancerologia de Mexico | Trial completion date: Jul 2025 --> Jul 2027 | Trial primary completion date: Jul 2024 --> Jul 2026

P1, N=33, Active, not recruiting, BeOne Medicines | N=93 --> 33 | Trial completion date: Apr 2028 --> May 2026 | Trial primary completion date: Apr 2028 --> May 2026 | Recruiting --> Active, not recruiting

P=N/A, N=74, Recruiting, Instituto Nacional de Cancerologia de Mexico | Trial completion date: Feb 2026 --> Feb 2027 | Trial primary completion date: Dec 2025 --> Dec 2026

P3, N=218, Completed, Sandoz | Suspended --> Completed