EGFR (Epidermal growth factor receptor)

P2, N=70, Recruiting, Innate Pharma | Trial completion date: Sep 2026 --> Jun 2027 | Trial primary completion date: Jun 2025 --> Jun 2027

P1/2, N=284, Active, not recruiting, Cullinan Therapeutics Inc. | Trial completion date: Mar 2026 --> Mar 2028 | Trial primary completion date: Jan 2026 --> Oct 2025

P=N/A, N=305, Active, not recruiting, Shanghai Chest Hospital | Recruiting --> Active, not recruiting | Trial completion date: Mar 2026 --> Dec 2027 | Trial primary completion date: Mar 2025 --> Dec 2026

Furthermore, static magnetic fields have been reported to increase apoptosis, inhibit proliferation, and may offer a complementary treatment with low toxicity. These findings suggest that magnetic-field-based approaches offer an innovative strategy for GBM treatment.

Additionally, co-treatment with the autophagy inhibitor chloroquine (CQ) attenuated MA-induced FTH1 downregulation and rescued MA-induced inhibition of cell viability in MDA-MB-231 cells...Bioinformatics analysis identified key hub genes associated with MA-induced autophagy, including tumor protein p53 (TP53), heat shock protein 90 alpha family class a member 1 (HSP90AA1), AKT serine/threonine kinase 1 (AKT1), mTOR, tumor necrosis factor (TNF), interleukin 6 (IL6), epidermal growth factor receptor (EGFR) and BCL2 apoptosis regulator (BCL2), as well as hub genes related to ferroptosis, such as mitogen-activated protein kinase 3 (MAPK3), RELA proto-oncogene (RELA), epidermal growth factor receptor (EGFR), prostaglandin-endoperoxide synthase 2 (PTGS2), SRC proto-oncogene (SRC), interleukin 1 beta (IL1B), interleukin 6 (IL6), and peroxisome proliferator activated receptor gamma (PPARG). In MDA-MB-231 cells, MA triggered autophagy through p53 upregulation and mTOR signaling inhibition, and induced ferroptosis by reprogramming GSH metabolism and activating the NCOA4-mediated ferritinophagy pathway, lead to FTH1 degradation.

Functional relevance of AKT signaling was evaluated using siRNA knockdown, MK2206, and SC79...EEDJF exerts anti-colorectal cancer effects in vitro, potentially associated with regulation of PI3K-Akt/p21 signaling. These findings provide a basis for further studies on the bioactive constituents, pharmacological mechanisms, and in vivo efficacy of DJF-derived preparations.

Initial studies were done by molecular docking of five analogs of quinazoline- quinazolinone hybrids, erlotinib, and doxorubicin against the epidermal growth factor receptor. The insertion of a nitro group at the 7 position of quinazolinone enhanced the cytotoxic efficacy against MCF-7 cells, likely attributable to electronic influences. Consequently, this compound could serve as a lead compound in the search for new classes of effective anticancer agents.

T790M-positive samples showed clearly higher measured DNA concentration values after hybridization (5.9-7.4 ng/µL; mean = 6.7 ± 0.6 ng/µL), whereas negative and control samples remained low (1.7-2.3 ng/µL), confirming the analytical specificity and reproducibility of the developed system.This platform offers a rapid, cost-effective, and portable approach for mutation detection without requiring complex instrumentation. The CNT-Fe3O4-probe nanoplatform demonstrates promising potential for future translation into liquid biopsy applications and personalized therapeutic monitoring in NSCLC.

Osimertinib dose reduction in the first-line setting was not associated with inferior OS, suggesting that appropriate dose modification helps maintain PS. Transition to BSC after progression, rather than initial dose intensity, was associated with poor prognosis.

This report of a patient with the rare p.(Cys797Ala) EGFR acquired mutation highlights the role of molecular modelling and IHC for phosphorylated proteins as tools to functionally characterize variants of unknown significance and help clinical decisions.