Filtered By:
Drug: Tarceva
Education: Study

This page shows you your search results in order of date.

Order by Relevance | Date

Total 33 results found since Jan 2013.

Heat shock protein 90 inhibitor 17-AAG down-regulates thymidine phosphorylase expression and potentiates the cytotoxic effect of tamoxifen and erlotinib in human lung squamous carcinoma cells
Biochem Pharmacol. 2022 Aug 9:115207. doi: 10.1016/j.bcp.2022.115207. Online ahead of print.ABSTRACTElevated thymidine phosphorylase (TP) levels, a key enzyme in the pyrimidine nucleoside salvage pathway, in cancer cells, are related to a poor prognosis in a variety of cancers. Heat shock protein 90 (Hsp90) is a ubiquitous molecular chaperone that is involved in the stabilization and maturation of many oncogenic proteins. The aim of this study is to elucidate whether Hsp90 inhibitor 17-AAG could enhance tamoxifen- and erlotinib-induced cytotoxicity in nonsmall cell lung cancer (NSCLC) cells via modulating TP expression in ...
Source: Biochemical Pharmacology - August 12, 2022 Category: Drugs & Pharmacology Authors: Jen-Chung Ko Jyh-Cheng Chen Jou-Min Hsieh Pei-Yu Tseng Chen-Shan Chiang Li-Ling Liu Chin-Cheng Chien I-Hsiang Huang Qiao-Zhen Chang Bo-Cheng Mu Yun-Wei Lin Source Type: research

Combination Therapy with PIK3R3-siRNA and EGFR-TKI Erlotinib Synergistically Suppresses Glioblastoma Cell Growth In Vitro
CONCLUSIONS: Our data propose that suppression of PIK3R3 can effectively triggers apoptosis and enhances the sensitivity of the glioblastoma cells to EGFR-TKI erlotinib. Thus, PIK3R3 can be a potential therapeutic target in glioblastoma patients.<br />.PMID:34967581 | DOI:10.31557/APJCP.2021.22.12.3993
Source: Asian Pacific Journal of Cancer Prevention - December 30, 2021 Category: Cancer & Oncology Authors: Razieh Amini Hadi Karami Mohammad Bayat Source Type: research

GLI1 activation is a key mechanism of erlotinib resistance in human non-small cell lung cancer.
Authors: Dong Z, Wang Y, Ding V, Yan X, Lv Y, Zhong M, Zhu F, Zhao P, He C, Ding F, Shi H Abstract Lung cancer is the leading cause of cancer-associated death worldwide. In recent years, the advancement of epidermal growth factor receptor-tyrosine kinase inhibitor (EGFR-TKI) targeted therapies has provided clinical benefits for lung cancer patients with EGFR mutations. The response to EGFR-TKI varies in patients with lung cancer, and resistance typically develops during the course of the treatment. Therefore, understanding biomarkers which can predict resistance to EGFR-TKI is important. Overexpression of GLI cause...
Source: Oncology Letters - September 1, 2020 Category: Cancer & Oncology Tags: Oncol Lett Source Type: research

Heterogeneity and Plasticity of Human Breast Cancer Cells in Response to Molecularly-Targeted Drugs
Non-responsive subpopulation of tumor cells, and acquired resistance in initially responsive cells are major challenges for cancer therapy with molecularly-targeted drugs. While point mutations are considered the major contributing factor to acquired resistance, in this study we explored the role of heterogeneity and plasticity of selected human breast cancer cell lines (MDA-MB-231, MDA-MB-468, and AU565) in their initial and adjusted response, respectively, to ruxolitinib, everolimus, and erlotinib. After determination of lethal concentration for 50% cell death (LC50), cells were exposed to selected drugs using three diff...
Source: Frontiers in Oncology - October 14, 2019 Category: Cancer & Oncology 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

YM155 sensitizes non-small cell lung cancer cells to EGFR-tyrosine kinase inhibitors through the mechanism of autophagy induction
In this study, we showed that YM155 markedly enhanced the sensitivity of erlotinib to EGFR-TKI resistant NSCLC cell lines H1650 (EGFR exon 19 deletion and PTEN loss) and A549 (EGFR wild type and KRAS mutation) through inducing autophagy-dependent apoptosis and autophagic cell death. The effects of YM155 combined with erlotinib on apoptosis and autophagy inductions were more obvious than those of YM155 in combination with survivin knockdown by siRNA transfection, suggesting that YM155 induced autophagy and apoptosis in the NSCLC cells partially depend on survivin downregulation. Meanwhile, we found that the AKT/mTOR pathway...
Source: Biochimica et Biophysica Acta (BBA) Molecular Basis of Disease - October 11, 2018 Category: Molecular Biology Source Type: research

Targeting autophagy by small molecule inhibitors of vacuolar protein sorting 34 (Vps34) improves the sensitivity of breast cancer cells to Sunitinib
In this study we systematically screened a library of 306 known anti-cancer drugs for their ability to induce autophagy using a cell-based assay. 114 of the drugs were classified as autophagy inducers; for 16 drugs, the cytotoxicity was potentiated by siRNA-mediated knock-down of Atg7 and Vps34. These drugs were further evaluated in breast cancer cell lines for autophagy induction, and two tyrosine kinase inhibitors, Sunitinib and Erlotinib, were selected for further studies.
Source: Cancer Letters - July 25, 2018 Category: Cancer & Oncology Authors: Matheus Dyczynski, Yasmin Yu, Magdalena Otrocka, Santiago Parpal, Tiago Braga, Aine Brigette Henley, Henric Zazzi, Mikael Lerner, Krister Wennerberg, Jenny Viklund, Jessica Martinsson, Dan Grand ér, Angelo De Milito, Katja Pokrovskaja Tamm Tags: Original Articles Source Type: research

Napsin A is negatively associated with EMT ‑mediated EGFR‑TKI resistance in lung cancer cells.
Napsin A is negatively associated with EMT‑mediated EGFR‑TKI resistance in lung cancer cells. Mol Med Rep. 2018 May 25;: Authors: Zhou L, Lv X, Yang J, Zhu Y, Wang Z, Xu T Abstract Epidermal growth factor receptor tyrosine kinase inhibitors (EGFR‑TKI) have been used as a standard therapy for patients with lung cancer with EGFR‑activating mutations. Epithelial‑mesenchymal transition (EMT) has been reported to be associated with the development of EGFR‑TKI resistance, which limits the clinical efficacy of EGFR‑TKI. Therefore, investigating the resistance‑associated mechanism is required i...
Source: Molecular Medicine Reports - June 2, 2018 Category: Molecular Biology Tags: Mol Med Rep Source Type: research

Novel drug-resistance mechanisms of pemetrexed-treated non-small cell lung cancer.
In this study, we explored new drug resistance mechanisms of PEM-treated NSCLC using two combinations of parental and PEM-resistant NSCLC cell lines from PC-9 and A549. PEM increased the apoptosis cells in parental PC-9 and the senescent cells in parental A549. However, such changes were not observed in the respective PEM-resistant cell lines. Quantitative RT-PCR analysis revealed that, besides an increased gene expression of thymidylate synthase in PEM-resistant PC-9 cells, the solute carrier family 19 member1 (SLC19A1) gene expression was markedly decreased in PEM-resistant A549 cells. The siRNA-mediated knockdown of SLC...
Source: Oncotarget - April 25, 2018 Category: Cancer & Oncology Tags: Oncotarget Source Type: research

Inositol trisphosphate receptor type 3-mediated enhancement of EGFR and MET co-targeting efficacy in non-small cell lung cancer detected by 18F-fluorothymidine.
CONCLUSIONS: Our findings indicate that 18F-FLT PET/CT is able to detect the enhanced efficacy of EGFR and MET inhibitors in oncogene-driven NSCLC and that such enhancement is mediated by IP3R3 through its interaction with K-Ras. PMID: 29618618 [PubMed - as supplied by publisher]
Source: Clinical Cancer Research - April 4, 2018 Category: Cancer & Oncology Authors: Iommelli F, De Rosa V, Terlizzi C, Monti M, Panico M, Fonti R, Del Vecchio S Tags: Clin Cancer Res 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

Estrogen receptor β1 activation accelerates resistance to epidermal growth factor receptor-tyrosine kinase inhibitors in non-small cell lung cancer.
In conclusion, ERβ1 was activated in EGFR-TKI secondary resistance. The downregulation of ERβ1 sensitized the cells to EGFR-TKIs. ERβ1 may be a key molecule in EGFR-TKI therapy. In addition, anti-ERβ1 treatment may reverse TKI resistance. PMID: 29328407 [PubMed - as supplied by publisher]
Source: Oncology Reports - January 14, 2018 Category: Cancer & Oncology Tags: Oncol Rep Source Type: research