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Investigation of the blood levels at a reduced dose of erlotinib with the addition of ritonavir compared to the normal dose of erlotinib

ABSTRACT: Primary objectives: Effect of the highly potent CYP3A4 inhibitor ritonavir on the pharmacokinetics (PK) of erlotinib, measured as AUC0-24h, AUCmean, Cmax and Cmin Primary endpoints: The effect of the highly potent CYP3A4 inhibitor ritonavir on the pharmacokinetics (PK) of erlotinib, measured as AUC0-24h, Cmax and Cmin.

DISEASE(S): Non-small Cell Lung Cancer Stage Iv,Advanced Egfr Mutation Positive Non Small Cell Lung Cancer, Pancreatic Carcinoma, Colorectal Cancer And Biliary Cancer,Gevorderd Egfr Mutatie Positief Niet-kleincellig Longkanker, Pancreascarcinoom, Colorectaal Kanker En Galwegkanker

PROVIDER: 2538815 | ecrin-mdr-crc |

REPOSITORIES: ECRIN MDR

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Charaterization of genetic alterations and gene expression signatures found in erlotinib-resistant and erlotinib/crizotinib dual-resistant HCC827 subpopulations

Project description:The non-small cell lung cancer (NSCLC) cell line HCC827 harbors an activating EGFR mutation (exon 19 deletion) that confers sensitivity to the FDA-approved EGFR inhibitor erlotinib. By applying the ClonTracer barcoding system, we were able to show the presence of pre-existing sub-populations in HCC827 that contribute to erlotinib resistance. Prior studies implicated that MET amplification confers resistance to erlotinib in this cell line. Therefore we examined the effects of the c-Met inhibitor crizotinib on the barcoded HCC827 population when treated either sequentially or simultaneously with both inhibitors. Despite the significant reduction in barcode complexity, the erlotinib/crizotinib combination treatment failed to eradicate all of the resistant clones implying the presence of an erlotinib/crizotinib dual resistant subpopulation. We performed transcriptome profiling (RNA-seq) to elucidate the potential resistance mechanisms of the dual resistant subpopulation in comparison to vehicle-treated or single agent erlotinib-resistant HCC827 cell populations as controls. mRNA profiling of the subpopulations of human NSCLC cell line HCC827 that contribute to EGFR inhibitor erlotinib and MET inhibitor crizotinib resistance

2014-10-07 | E-GEOD-62118 | biostudies-arrayexpress

Charaterization of genetic alterations and gene expression signatures found in erlotinib-resistant and erlotinib/crizotinib dual-resistant HCC827 subpopulations

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Differential Gene Expression in Erlotinib-Treated Fibroblasts

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Gene expression profiling of erlotinib-resistant PC9 cells.

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microRNA profiling of H358 non-small cell lung cancer cells selected for resistance against erlotinib or wild-type

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Quinacrine Overcomes Resistance to Erlotinib by Inhibiting FACT, Nuclear Factor-kappa B and Cell Cycle Progression in Non-Small Cell Lung Cancer

Project description:Erlotinib is a tyrosine kinase inhibitor (TKI) that is approved as a second-line monotherapy in patients with advanced non-small cell lung cancer (NSCLC). In these patients, erlotinib prolongs survival but its benefit remains modest since many tumors express wild-type EGF receptor (wtEGFR) lacking a TKI-sensitizing mutation, develop a second-site EGFR mutation, e.g., EGFR-L858R/T790M, or activate an alternate receptor tyrosine kinase, e.g., through MET amplification. To test potential drug combinations that could improve the efficacy of erlotinib, we combined erlotinib with quinacrine, which inhibits the FACT (facilitates chromatin transcription) complex that is required for nuclear factor-κB (NF-κB) transcriptional activity. In A549 (wtEGFR), H1975 (EGFR-L858R/T790M) and H1993 (MET amplification) NSCLC cells, the combination of erlotinib and quinacrine was highly synergistic, as quantified by Chou-Talalay combination indices. The combination inhibited colony formation, induced cell cycle arrest and apoptosis, and slowed xenograft tumor growth. Quinacrine decreased the level of active FACT subunit SSRP1 and suppressed NF-κB-dependent luciferase activity. Knockdown of SSRP1 decreased cell growth and sensitized cells to erlotinib. Transcriptomic profiling showed that quinacrine, alone or in combination with erlotinib, significantly affected cell cycle-related genes that contain binding sites for transcription factors that regulate SSRP1 target genes. As potential biomarkers of drug synergy, we identified genes that were more strongly suppressed by the combination than by either single treatment, and whose increased expression predicted poorer survival in lung adenocarcinoma patients. Combination of quinacrine and erlotinib is synergistic in NSCLC through suppression of FACT, resulting in inhibition of cell cycle progression.

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