gefitinib

This ADP-ribosylation-based prognostic model reliably predicts LUAD survival and identifies potential biomarkers for tailored therapy.

Notably, artificial catalysts lacking spatial confinement exhibit higher defluorination efficiency. This work reveals that biological spatial confinement reshapes reaction pathways and modulates activation barriers, thereby deepening the mechanistic understanding of fluorinated drug metabolism and supporting rational design for safer pharmaceuticals and environmentally benign detoxification strategies.

After propensity score matching (n=412), these differences persisted for treatment duration (12.9 vs. 6.8 months), CNS-rPFS (24.9 vs. 14.5 months), and OS (25.6 vs. 14.6 months), all P<0.001. In real-world practice, osimertinib is associated with longer first-line treatment duration, improved CNS control, and longer survival compared with gefitinib among EGFR-positive mNSCLC patients with brain metastases.

Here, we established gefitinib- and osimertinib-resistant NSCLC cells and found that NSUN2 knockdown did not affect proliferation or drug sensitivity under immunodeficient conditions. Consistently, TRIM29 depletion phenocopied NSUN2 knockdown by promoting M1 polarization and macrophage migration. These findings identify NSUN2 as a driver of immune evasion and acquired EGFR-TKI resistance through epigenetic regulation of macrophage infiltration and polarization.

Nanoparticles such as liposomes, lactoferrin-based specialized nanocarriers, and gold nanoparticles functionalized with targeting ligands including Pep-1L, lactoferrin, and RGD peptides, and loaded with anticancer drugs such as temozolomide, gefitinib, and epirubicin, are being explored for targeted GBM therapy. This highlights the need for future research focused on developing biodegradable and biocompatible nanomaterials, along with optimized ligand-guided designs, to improve safety and enhance translational feasibility in glioblastoma therapy. Literature search Methodology: &lsqb;PubMed and Google Scholar; 2006-2026].

We report a 59-year-old female non-smoker with stage IV EGFR Leu858Arg-mutated lung adenocarcinoma who sequentially received first-line osimertinib (~9 months), second-line osimertinib plus savolitinib for MET amplification (~20 months), third-line platinum-based chemotherapy with local ablative therapy for oligo-progression, and fourth-line docetaxel. This case illustrates that an acquired BRAF fusion may emerge as a potentially targetable bypass alteration in EGFR-mutated MET-amplified NSCLC after progression on combined EGFR-MET inhibition and that the combination of a first-generation EGFR-TKI and a MEK inhibitor can be associated with prolonged systemic disease control. The findings are hypothesis-generating and support the value of CGP at sequential progression points to guide mechanism-based therapy in oncogene-driven NSCLC.

This case demonstrates the effectiveness of first-generation TKIs in treating metastatic EGFR-positive NSCLC, particularly in countries that cannot afford recent targeted therapies. In addition, it describes a rare adverse effect that was well tolerated and managed successfully.

P1/2, N=6, Completed, Stanford University | N=12 --> 6

Antioxidant N-acetylcysteine (NAC) treatment markedly restored GSH content and suppressed lipid ROS overproduction to relieve AO-triggered ferroptosis. The introduction of the iron scavenger deferoxamine or the ferroptosis inhibitor ferrostatin-1 weakened AO-induced ferroptosis in breast cancer cells...Selective EGFR inhibitor gefitinib exacerbated AO-mediated ferroptosis and autophagy, while genetic overexpression of EGFR completely reversed these AO-mediated phenotypes...Our study revealed that AO facilitated autophagy-dependent ferroptosis in breast cancer cells through the downregulation of EGFR. This work provides a new perspective on the antitumor activity of AO, which is valuable for further investigations of the practical application of AO in breast cancer.

P2, N=156, Completed, European Organisation for Research and Treatment of Cancer - EORTC | Active, not recruiting --> Completed | Trial completion date: Dec 2027 --> Aug 2025

HDI inhibits breast cancer growth and lung metastasis by dual targeting of PTK2B and CCN2, thereby suppressing KRAS-p38 MAPK signaling, reversing EMT, and modulating TIMP2/MMP2-mediated extracellular matrix remodeling. Asperulosidic acid is identified as an important active constituent contributing to these effects. The favorable safety profile of HDI and its synergistic interaction with gefitinib support its potential application as a multitarget adjuvant therapy for metastatic breast cancer, particularly TNBC.

This is the first report of pulmonary adenocarcinoma with both high serum β-hCG levels and an EGFR mutation.