gefitinib

Importantly, miR-23c mimic re-sensitized NSCLC-resistant cells to gefitinib, whereas the combination of miR-23c mimic with a neutralizing IL-6R antibody potentiated the sensitivity to the drug. Collectively, our data demonstrated that miR-23c acts as a tumor suppressor in NSCLC cell lines carrying EGFR mutations and that the axis miR-23c/IL-6R might represent a potential target for the development of therapeutic approaches to overcome resistance to gefitinib.

Drug sensitivity analysis suggested gefitinib, zebularine, and simvastatin as potential therapies for high-risk AML (p < 0.05). Notably, in vitro studies indicated that KCNMB1 facilitates AML progression. In conclusion, our robust PRG-based model elucidates the link between platelet biology, immune dysregulation, and therapeutic vulnerability in AML, offering clinical utility for risk stratification and treatment decisions.

The mOS of the EGFR-TP53 co-mutant group who received second-line TKIs combined with platinum-containing double-drug chemotherapy and bevacizumab after the progression of first-line single-drug TKIs was 27.0 months versus 6.0 months compared with those who did not receive second-line therapy (P = .019). In first-line EGFR-TKIs monotherapy in patients with EGFR-TP53 co-mutation, osimertinib was clearly superior to gefitinib. In first-line EGFR-TKIs monotherapy progression, TKIs combined with chemotherapy and antiangiogenesis therapy could prolong patients' survival.

According to cytotoxicity test results, it was determined that compound 4j showed high inhibitory activity compared to cisplatin and gefitinib in the A549 cell line. In EGFR enzyme inhibition studies, it was observed that the activities of molecules 4b, 4f, and 4j were higher than gefitinib. In silico studies indicated that 4j interacted by establishing significant bonds with both caspase-3 and EGFR enzyme.

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