Search results for "ERLOTINIB"
showing 10 items of 52 documents
P3.02c-046 Safety, Clinical Activity and Biomarker Results from a Phase Ib Study of Erlotinib plus Atezolizumab in Advanced NSCLC
2017
MA15.02 Long-Term Safety and Clinical Activity Results from a Phase Ib Study of Erlotinib Plus Atezolizumab in Advanced NSCLC
2018
Surface plasmon resonance signal enhancement based on erlotinib loaded magnetic nanoparticles for evaluation of its interaction with human lung cance…
2021
Abstract Surface plasmon resonance (SPR) sensor provides a very useful tool based on its label-free, real-time monitoring and low price properties. However, measurement of small molecules and extremely diluted analytes is difficult and therefore, signal enhancement is required. In the present study, signal enhancement of erlotinib conjugated magnetic nanoparticles (erlotinib-MNPs) compared to erlotinib was evaluated via their interaction with overexpressed epidermal growth factor receptor on human lung cancer cells (A549 cell line) surface using SPR sensor at three temperature levels. The attained results showed an average signal amplification of about 2.5-fold for MNP-erlotinib interaction…
Cytotoxicity of the indole alkaloid reserpine from Rauwolfia serpentina against drug-resistant tumor cells.
2015
Abstract Background: The antihypertensive reserpine is an indole alkaloid from Rauwolfia serpentina and exerts also profound activity against cancer cells in vitro and in vivo. The present investigation was undertaken to investigate possible modes of action to explain its activity toward drug-resistant tumor cells. Material and methods: Sensitive and drug-resistant tumor cell lines overexpressing P-glycoprotein (ABCB1/MDR1), breast cancer resistance protein (ABCG2/BCRP), mutation-activated epidermal growth factor receptor (EGFR), wild-type and p53-knockout cells as well as the NCI panel of cell lines from different tumor origin were analyzed. Reserpine's cytotoxicity was investigated by res…
Evaluation of erlotinib treatment response in non-small cell lung cancer using metabolic and anatomic criteria
2016
BACKGROUND: In this paper the clinical value of PET for early prediction of tumor response to erlotinib in patients with advanced or metastatic non-small cell lung cancer (NSCLC) after failure of at least one prior chemotherapy regimen is evaluated. The aim was to compare the early metabolic treatment response using European Organization for Research and Treatment of Cancer (EORTC) 1999 recommendations and PET Response Criteria in Solid Tumors (PERCIST), and the standard treatment response using Response Evaluation Criteria in Solid Tumors (RECIST). METHODS: Twenty patients with stage IV NSCLCwere enrolled prospectively. PET/CT studies were performed before, then 48 hours, and 45 days after…
Treatment Monitoring Program for Implementation of Adherence to Second-Line Erlotinib for Advanced Non–Small-Cell Lung Cancer
2012
Abstract Background Adherence to erlotinib could be a determinant for clinical outcome and treatment toxicity in patients with advanced non–small-cell lung cancer (A-NSCLC). Patients and Methods In an observational study, the Basel Assessment of Adherence Scale (BAAS), a visual analogue scale (VAS), pill counting, and missed appointment rate were used to evaluate adherence in a first cohort of patients who was prescribed erlotinib without a specifically designed management strategy and in a second cohort of patients followed by an oral treatment monitoring program. Results Adherence > 95% by BAAS at 2 months of treatment in the first and second cohorts was 72% and 84%, respectively ( P = .0…
Abstract LB-399: Chronic inhibition of mutant EGFR in NSCLC leads to EGFR TKI resistance by TGF-β1 mediated epithelial to mesenchymal transition
2011
Abstract In NSCLC, activating EGFR mutations underlie responsiveness of NSCLCs to reversible EGFR tyrosine kinase inhibitors (TKIs), including gefitinib and erlotinib. Despite initial responses, acquired resistance invariably develops, mediated by the emergence of the secondary T790M mutation and by focal amplification of MET, in approximately 50% and 30% of patients, respectively. The resistance mechanisms for the remaining 20% of cases remain elusive. EGFR TKI-sensitive HCC827 cells were exposed to graded concentrations of erlotinib for 6 months. Approximately 70% of the isolated clones were resistant to erlotinib and harbored MET amplification, and were sensitive to dual EGFR/MET inhibit…
Temporal molecular and biological assessment of an erlotinib-resistant lung adenocarcinoma model reveals markers of tumor progression and treatment r…
2012
Abstract Patients with lung cancer with activating mutations in the EGF receptor (EGFR) kinase, who are treated long-term with tyrosine kinase inhibitors (TKI), often develop secondary mutations in EGFR associated with resistance. Mice engineered to develop lung adenocarcinomas driven by the human EGFR T790M resistance mutation are similarly resistant to the EGFR TKI erlotinib. By tumor volume endpoint analysis, these mouse tumors respond to BIBW 2992 (an irreversible EGFR/HER2 TKI) and rapamycin combination therapy. To correlate EGFR-driven changes in the lung with response to drug treatment, we conducted an integrative analysis of global transcriptome and metabolite profiling compared wit…
Abstract 766: Suppression of gefitinib-induced EMT in EGFR mutant NSCLC preferentially selects for acquired T790M
2015
Abstract Activating EGFR mutations in non-small lung cancer (NSCLC) confer sensitivity to reversible EGFR tyrosine kinase inhibitors (TKIs), including gefitinib and erlotinib. Despite promising initial response acquired resistance develops mediated by the emergence of the secondary T790M mutation or by focal amplification of MET. An epithelial-to-mesenchymal transition (EMT) is clinically linked to NSCLCs with acquired EGFR TKI resistance. The exact mechanisms of EGFR TKI resistance with EMT phenotype remain elusive; therefore, we attempted to develop a strategy to prevent the emergence of EGFR TKI resistance with EMT phenotype. In order to mimic the development of acquired EGFR TKI resista…