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Cancer: Lung Cancer
Drug: Tarceva

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Total 32 results found since Jan 2013.

Inhibition of the effect of epidermal growth factor (EGF) on lung cancer cells. The use of plasmids encoding specific siRNA molecules
Conclusions: The inhibition of EGF system blockade with siRNA technique appears to be more effective strategy in cancer treatment in vitro, as compared to erlotinib, since this effect is probably EGFR gene mutation-independent. However, we have not definitively proved if it resulted in increased tumor cell immunogenicity.
Source: European Respiratory Journal - October 30, 2015 Category: Respiratory Medicine Authors: Gawronski, M., Kopinski, P., Jankowski, M., Goede, A., Szpechcinski, A., Chorostowska, J. Tags: 11.1 Lung Cancer Source Type: research

Antitumor activity of kinetochore-associated protein 2 siRNA against lung cancer patient-derived tumor xenografts.
Authors: Makita Y, Teratani M, Murata S, Hoashi Y, Matsumoto S, Kawamata Y Abstract It has been widely reported that patient-derived tumor xenografts (PDXs) are more similar to tumor tissues than conventional cancer cell lines. Kinetochore-associated protein 2 (KNTC2) is known to be upregulated specifically in tumor tissues of cancer patients and is recognized as a potential target for cancer therapy. Previously, in vivo antitumor activities of KNTC2 short interfering RNA encapsulated into a lipid nanoparticle (KNTC2-LNP) were reported in orthotopic hepatocellular carcinoma mouse models. However, it remains unclear...
Source: Oncology Letters - March 16, 2018 Category: Cancer & Oncology Tags: Oncol Lett Source Type: research

Inhibition of SMYD2 Sensitized Cisplatin to Resistant Cells in NSCLC Through Activating p53 Pathway
In conclusion, the present study elucidated that the activity of SMYD2 in NSCLC may affect the cell sensitivity to chemotherapeutic agents, especially to CDDP. The elevated SMYD2 mediated CDDP resistance and malignant phenotype in NSCLC, indicating that SMYD2 may be a useful biomarker of CDDP resistance in NSCLC. Inhibition of SMYD2 contributes to the methylation-related activation of p53 and thus results in cell apoptosis. Furthermore, combination treatment with CDDP and an SMYD2 inhibitor had a synergistically antitumor effects in a xenograft model in vivo. Given that SMYD2 has reversible effects and is a targetable prot...
Source: Frontiers in Oncology - April 25, 2019 Category: Cancer & Oncology Source Type: research

YAP promotes erlotinib resistance in human non-small cell lung cancer cells.
Authors: Hsu PC, You B, Yang YL, Zhang WQ, Wang YC, Xu Z, Dai Y, Liu S, Yang CT, Li H, Hu B, Jablons DM, You L Abstract Yes-associated protein (YAP) is a main mediator of the Hippo pathway, which promotes cancer development. Here we show that YAP promotes resistance to erlotinib in human non-small cell lung cancer (NSCLC) cells. We found that forced YAP overexpression through YAP plasmid transfection promotes erlotinib resistance in HCC827 (exon 19 deletion) cells. In YAP plasmid-transfected HCC827 cells, GTIIC reporter activity and Hippo downstream gene expression of AREG and CTGF increased significantly (P<0.0...
Source: Oncotarget - July 15, 2016 Category: Cancer & Oncology Tags: Oncotarget Source Type: research

Inhibition of Hedgehog signaling sensitizes NSCLC cells to standard therapies through modulation of EMT-regulating miRNAs
Conclusions: We demonstrate that Hh pathway, through EMT-induction, leads to reduced sensitivity to EGFR-TKIs in NSCLCs. Therefore, targeting Hh pathway may lead to the reversal of EMT phenotype and improve the therapeutic efficacy of EGFR-TKIs in NSCLC patients.
Source: Journal of Hematology and Oncology - October 7, 2013 Category: Hematology Authors: Aamir AhmadMa¿in MaitahKevin GinnebaughYiwei LiBin BaoShirish GadgeelFazlul Sarkar Source Type: research

AXL and MET Inhibition in Resistance to EGFR Inhibitor
In this study, we investigated the antitumor activity of NPS-1034, a newly developed drug that targets both MET and AXL, in NSCLC cells with acquired resistance to gefitinib or erlotinib (HCC827/GR and HCC827/ER, respectively). Characterization of H820 cells and evaluation of NPS-1034 efficacy in these cells were also performed. The resistance of HCC827/GR was mediated by MET activation, whereas AXL activation led to resistance in HCC827/ER. The combination of gefitinib or erlotinib with NPS-1034 synergistically inhibited cell proliferation and induced cell death in both resistant cell lines. Accordingly, suppression of Ak...
Source: Cancer Research - January 5, 2014 Category: Cancer & Oncology Authors: Rho, J. K., Choi, Y. J., Kim, S. Y., Kim, T. W., Choi, E. K., Yoon, S.-J., Park, B. M., Park, E., Bae, J. H., Choi, C.-M., Lee, J. C. Tags: Therapeutics, Targets, and Chemical Biology Source Type: research

Effect of simvastatin on the resistance to EGFR tyrosine kinase inhibitors in a non-small cell lung cancer with the T790M mutation of EGFR.
This study investigated overcoming resistance to EGFR-TKI using simvastatin. We demonstrated that addition of simvastatin to gefitinib enhanced caspase-dependent apoptosis in T790M mutant NSCLC cells. Simvastatin also strongly inhibited AKT activation, leading to suppression of β-catenin activity and the expression of its targets, survivin and cyclin D1. Both insulin treatment and AKT overexpression markedly increased p-β-catenin and survivin levels, even in the presence of gefitinib and simvastatin. However, inhibition of AKT by siRNA or LY294002 treatment decreased p-β-catenin and survivin levels. To determine the rol...
Source: Experimental Cell Research - March 12, 2014 Category: Cytology Authors: Hwang KE, Kwon SJ, Kim YS, Park DS, Kim BR, Yoon KH, Jeong ET, Kim HR Tags: Exp Cell Res Source Type: research

Abstract 856: Combination of crizotinib and radiation in the treatment of ALK-positive and cetuximab-resistant lung cancer
We examined the effect of crizotinib in combination with radiation on ALK signaling, cell proliferation, cell cycle distribution and radiosensitivity in ALK-positive NSCLC cell lines H3122 and H2228 in vitro. We also examined the in-vivo effects of crizotinib in combination with radiation in H3122 and H2228 xenograft models. Crizotinib blocked phosphorylation of ALK and its downstream effectors and inhibited cell proliferation in a dose-dependent manner. The combination of crizotinib and radiation resulted in increased inhibition of cell growth. Although cells were sensitized to radiation by crizotinib, molecular knockdown...
Source: Cancer Research - September 30, 2014 Category: Cancer & Oncology Authors: Li, C., Huang, S., Walters, N., Armstrong, E. A., Harari, P. M. Tags: Clinical Research (Excluding Clinical Trials) Source Type: research

Mistletoe (viscum album) extract targets Axl to suppress cell proliferation and overcome cisplatin- and erlotinib-resistance in non-small cell lung cancer cells.
Conclusion : Taken together, our data provide that VAE targets Axl to suppress cell proliferation and to circumvent cisplatin- and erlotinib-resistance in NSCLC cells. Graphical abstract
Source: Phytomedicine - September 29, 2017 Category: Drugs & Pharmacology Source Type: research

Abstract 774: EGFR-regulated RGS expression contributes to paclitaxel resistance in human lung cancer cells
Lung cancer is one of the main causes of cancer-related death worldwide, and the 5-year survival of lung cancer is less than 20%. Paclitaxel is a widely used chemotherapeutic agent to treat a variety of cancers, but its therapeutic efficacy tends to be limited due to the development of drug resistance, raising the need to understand the molecular mechanisms underlying paclitaxel resistance. In the current study, we investigated the mechanisms of paclitaxel resistance in non-small cell lung cancers (NSCLCs). First, we established paclitaxel-resistant NSCLC cell lines, including H460 TxR and SK-MES TxR, by pulse- or prolonge...
Source: Cancer Research - September 30, 2014 Category: Cancer & Oncology Authors: Park, S.-H., Sung, M.-A., Lee, H.-Y. Tags: Experimental and Molecular Therapeutics Source Type: research

Abstract 2762: Akt kinase-interacting protein1, a novel therapeutic target for lung cancer with EGFR-activating and gatekeeper mutations
Epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs), such as gefitinib and erlotinib, show favorable effects in EGFR mutant lung cancer. However, responders eventually develop acquired resistance almost without exception, and secondary T790M mutations in EGFR account for approximately 50% of the acquired resistance. Recent studies indicated that EGFR mutant lung cancer cells are dependent on EGFR/Akt signaling for survival even after acquired T790M secondary mutation. Akt kinase-interacting protein1 (Aki1) is a scaffold protein that binds to wild-type EGFR after EGF ligand stimulation, maintains signa...
Source: Cancer Research - September 30, 2014 Category: Cancer & Oncology Authors: Yamada, T., Carbone, D. P., Takeuchi, S., Fujita, N., Yano, S. Tags: Experimental and Molecular Therapeutics Source Type: research

Radiosensitization of NSCLC cells by EGFR inhibition is the result of an enhanced p53-dependent G1 arrest.
CONCLUSION: For NSCLC cells increase in radiosensitivity by EGFR inhibition results from enhanced G1-arrest. However, this effect does not lead to improved tumor control because cells can be released from this arrest by re-stimulation. PMID: 25796091 [PubMed - as supplied by publisher]
Source: Radiotherapy and Oncology : journal of the European Society for Therapeutic Radiology and Oncology - March 18, 2015 Category: Radiology Authors: Kriegs M, Gurtner K, Can Y, Brammer I, Rieckmann T, Oertel R, Wysocki M, Dorniok F, Gal A, Grob TJ, Laban S, Kasten-Pisula U, Petersen C, Baumann M, Krause M, Dikomey E Tags: Radiother Oncol Source Type: research

Combined effects of EGFR tyrosine kinase inhibitors and vATPase inhibitors in NSCLC cells.
Abstract Despite excellent initial clinical responses of non-small cell lung cancer (NSCLC) patients to epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs), many patients eventually develop resistance. According to a recent report, vacuolar H+ ATPase (vATPase) is overexpressed and is associated with chemotherapy drug resistance in NSCLC. We investigated the combined effects of EGFR TKIs and vATPase inhibitors and their underlying mechanisms in the regulation of NSCLC cell death. We found that combined treatment with EGFR TKIs (erlotinib, gefitinib, or lapatinib) and vATPase inhibitors (bafilo...
Source: Toxicology and Applied Pharmacology - May 14, 2015 Category: Toxicology Authors: Jin HO, Hong SE, Kim CS, Park JA, Kim JH, Kim JY, Kim B, Chang YH, Hong SI, Hong YJ, Park IC, Lee JK Tags: Toxicol Appl Pharmacol Source Type: research

Abstract 2558: The mechanistic study on the effect of platinum-based chemotherapy efficacy imposed by EGFR-TKI regulated ERCC1 in non-small cell lung cancer (NSCLC)
Platinum-based chemotherapy is conventionally the first line treatment for EGFR wild type patients while EGFR-TKI is the standard for patients with mutation. Subgroup biomarker studies conducted in FASTACT-2 (Wu et al Lancet Oncology 2013) indicated that patients with positive ERCC1 attained longer overall survival and progression free survival under intercalated chemotherapy and EGFR-TKI, in comparison with solely chemotherapy. EGFR-TKI is postulated to down-regulate ERCC1 expression in EGFR wild type NSCLC cells, hence enhancing the Chemo efficacy. The study aims to investigate the missing link between EGFR and ERCC1 in ...
Source: Cancer Research - August 2, 2015 Category: Cancer & Oncology Authors: Cheong, H. T., Hui, C. W. C., Xu, F., Mok, T. S. K., Wong, C. H. Tags: Experimental and Molecular Therapeutics Source Type: research

Abstract 3576: Rictor alterations elicit non-canonical signaling mechanisms contributing to tumorigenicity and therapeutic resistance in non-small cell lung cancer (NSCLC)
Conclusion: Rictor alterations may define a new molecular NSCLC subtype with distinct biology that expose unique avenues for therapeutic intervention. Ongoing studies are underway to explore specific therapeutic strategies, non-canonical signaling and Rictor mutations.Supported by: NHI-NCI CA155196 2015 Apr 18-22; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(15 Suppl):Abstract nr 3576. doi:10.1158/1538-7445.AM2015-3576
Source: Cancer Research - August 2, 2015 Category: Cancer & Oncology Authors: Ruder, D., Papadimitrakopoulou, V., Shien, K., Kalhor, N., Lee, J. J., Hong, W. K., Tang, X., Girard, L., Minna, J. D., Diao, L., Wang, J., Hanson, N. E., Sun, J., Miller, V., Frampton, G., Herbst, R. S., Wistuba, I. I., Izzo, J. G. Tags: Experimental and Molecular Therapeutics Source Type: research