EGFR mutation

P3, N=98, Active, not recruiting, AstraZeneca | Trial completion date: Jun 2026 --> Jun 2027

P2, N=22, Completed, National Taiwan University Hospital | Active, not recruiting --> Completed | Trial completion date: Dec 2024 --> Feb 2026 | Trial primary completion date: Dec 2024 --> Feb 2026

Mechanistically, galangin suppressed M2 macrophage polarization, directly interacted with the efferocytosis-related targets CAMK2A and MERTK, and reduced their expression. Together, these findings establish efferocytosis as a novel and targetable vulnerability in drug-resistant NSCLC and highlight galangin as a promising sensitizer for overcoming resistance to two major targeted therapies.

A previous analysis of the RELAY phase 3 liquid biopsy addendum demonstrated suppressed EGFR-activating mutation allele count, increased total cell-free DNA (cfDNA) concentration, and shortened cfDNA fragment size with ramucirumab (RAM) plus erlotinib (ERL) versus placebo (PL) plus ERL in patients with EGFR-mutated NSCLC. This updated analysis revealed differences in total cfDNA concentration and T790M mutation rates between ex19del and L858R. RAM plus ERL may exhibit greater antitumor effects on L858R, supporting the favorable survival benefits observed previously in patients with a L858R.

The sequential multibiomarker algorithm achieved 96.5% sensitivity and 98.7% specificity for malignant PE detection, with 85.3% overall three-way classification accuracy. Multiomics integration combining proteomic biomarkers with single-cell immune profiling and genomic mutation characterization achieves high diagnostic accuracy for pleural effusion while revealing disease-specific immune mechanisms and mutation-driven therapeutic opportunities.

Chemo-immunotherapy with or without VEGFi may produce a modest survival improvement in select patients with EGFR-mutated NSCLC compared with chemotherapy. Identifying biomarkers able to predict a clinically meaningful benefit is warranted.

First-line Osimertinib induced a dramatic clinical and radiological response within days...This case underscores the critical difficulty of diagnosing lepidic-patterned tumors in an oncological emergency. It highlights the necessity of a multidisciplinary approach, combining cytology, radiology, and early molecular testing as a surrogate for traditional histopathology to guide urgent targeted therapy.

Understanding these dynamics is essential for developing targeted public health strategies that address the unique challenges faced by this population, balancing their cultural heritage with the realities of modern American life. Further analysis and wider scope studies are necessary to explore the implications of these findings on health outcomes.

Gefitinib and osimertinib, the first-generation and third-generation EGFR-TKI, have shown promising results in patients with EGFR-mutated lung cancer in clinical treatment. Moreover, PDK1 inhibitor JX06 rendered cancer cells more sensitive to gefitinib treatment in vivo, and JX06 and gefitinib combination treatments have a synergic effect to inhibit tumor growth. In conclusion, the KDM3A/METTL16/PDK1 axis plays an important role in cancer development and TKI resistance, which may offer new prognostic biomarkers and therapeutic targets for TKI resistance in the future.

In conclusion, extracranial metastasis, PLR and ECOG PS were identified to be prospective independent clinical prognostic indicators of survival in patients with lung adenocarcinoma and LM. Overall, the present study highlighted the potential use of clinical characteristics and hematological variables before treatment to predict the outcomes of patients with lung adenocarcinoma complicated with LM.

The association between the docking predictions and clinical outcomes corroborates the utility of computational modeling for tailoring therapies, although the structural models provide mechanistic insight into drug efficacy against these rare mutations. The present integrated approach emphasizes the value of merging in silico methods into clinical decision-making to overcome the therapeutic uncertainty of uncommon oncogenic driver alterations.

This report adds an insight into the involvement of genetic events in histological transformation in EGFR-mutated lung cancer.