The pan-HDAC inhibitor panobinostat acts as a sensitizer for erlotinib activity in EGFR-mutated and -wildtype non-small cell lung cancer cells
暂无分享,去创建一个
M. Lübbert | I. Schiffmann | J. Schüler | D. Pfeifer | G. Greve | M. Pantić
[1] Yang Xie,et al. Phase 1 study of romidepsin plus erlotinib in advanced non-small cell lung cancer. , 2015, Lung cancer.
[2] K. Politi,et al. The Next Wave of EGFR Tyrosine Kinase Inhibitors Enter the Clinic. , 2015, Cancer cell.
[3] M. Lübbert,et al. Epigenetic priming of non-small cell lung cancer cell lines to the antiproliferative and differentiating effects of all-trans retinoic acid , 2015, Journal of Cancer Research and Clinical Oncology.
[4] S. Belinsky,et al. SGI‐110 and entinostat therapy reduces lung tumor burden and reprograms the epigenome , 2014, International journal of cancer.
[5] G. Bepler,et al. A Phase I, Pharmacokinetic, and Pharmacodynamic Study of Panobinostat, an HDAC Inhibitor, Combined with Erlotinib in Patients with Advanced Aerodigestive Tract Tumors , 2014, Clinical Cancer Research.
[6] M. Fukuda,et al. Phase II trial of erlotinib in patients with advanced non-small-cell lung cancer harboring epidermal growth factor receptor mutations: additive analysis of pharmacokinetics , 2013, Cancer Chemotherapy and Pharmacology.
[7] M. Lübbert,et al. Epigenetic Priming of AML Blasts for All-trans Retinoic Acid-Induced Differentiation by the HDAC Class-I Selective Inhibitor Entinostat , 2013, PloS one.
[8] G. Giaccone,et al. Erlotinib versus docetaxel as second-line treatment of patients with advanced non-small-cell lung cancer and wild-type EGFR tumours (TAILOR): a randomised controlled trial. , 2013, The Lancet. Oncology.
[9] C. Moskaluk,et al. Phase I Trial of Induction Histone Deacetylase and Proteasome Inhibition Followed by Surgery in Non–Small-Cell Lung Cancer , 2012, Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer.
[10] F. Hirsch,et al. Randomized phase II trial of erlotinib with and without entinostat in patients with advanced non-small-cell lung cancer who progressed on prior chemotherapy. , 2012, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.
[11] David C. Smith,et al. Phase I study of vorinostat (suberoylanilide hydroxamic acid, NSC 701852) in combination with docetaxel in patients with advanced and relapsed solid malignancies , 2012, Investigational New Drugs.
[12] C. Plass,et al. Effects of Histone Deacetylase Inhibitors on Modulating H3K4 Methylation Marks - A Novel Cross-Talk Mechanism between Histone-Modifying Enzymes. , 2011, Molecular and cellular pharmacology.
[13] M. Lübbert,et al. The HDAC class I-specific inhibitor entinostat (MS-275) effectively relieves epigenetic silencing of the LAT2 gene mediated by AML1/ETO , 2011, Oncogene.
[14] Yihong Ma,et al. Histone Deacetylase Inhibitors Downregulate Checkpoint Kinase 1 Expression to Induce Cell Death in Non-Small Cell Lung Cancer Cells , 2010, PloS one.
[15] Y. Maehara,et al. Reciprocal and Complementary Role of MET Amplification and EGFR T790M Mutation in Acquired Resistance to Kinase Inhibitors in Lung Cancer , 2010, Clinical Cancer Research.
[16] M. Lübbert,et al. Histone deacetylase (HDAC) inhibitors in recent clinical trials for cancer therapy , 2010, Clinical Epigenetics.
[17] T. Mok,et al. Gefitinib or carboplatin-paclitaxel in pulmonary adenocarcinoma. , 2009, The New England journal of medicine.
[18] L. Garraway,et al. Oncogenic Activating Mutations Are Associated with Local Copy Gain , 2009, Molecular Cancer Research.
[19] B. Aggarwal,et al. Epidermal growth factor (EGF) activates nuclear factor-κB through IκBα kinase-independent but EGF receptor-kinase dependent tyrosine 42 phosphorylation of IκBα , 2007, Oncogene.
[20] S. Gery,et al. Histone deacetylase inhibitor, suberoylanilide hydroxamic acid (Vorinostat, SAHA) profoundly inhibits the growth of human pancreatic cancer cells , 2007, International journal of cancer.
[21] C. Bradbury,et al. Cross-talk between Histone Modifications in Response to Histone Deacetylase Inhibitors , 2007, Journal of Biological Chemistry.
[22] Chan Zeng,et al. Baseline Gene Expression Predicts Sensitivity to Gefitinib in Non–Small Cell Lung Cancer Cell Lines , 2006, Molecular Cancer Research.
[23] J. Minna,et al. Restoring E-cadherin expression increases sensitivity to epidermal growth factor receptor inhibitors in lung cancer cell lines. , 2006, Cancer research.
[24] Srinivas Annavarapu,et al. Combination of the histone deacetylase inhibitor LBH589 and the hsp90 inhibitor 17-AAG is highly active against human CML-BC cells and AML cells with activating mutation of FLT-3. , 2005, Blood.
[25] Patricia L. Harris,et al. Activating mutations in the epidermal growth factor receptor underlying responsiveness of non-small-cell lung cancer to gefitinib. , 2004, The New England journal of medicine.
[26] D. R. Lewis,et al. Cancer survival and incidence from the Surveillance, Epidemiology, and End Results (SEER) program. , 2003, The oncologist.
[27] Robert M. Gemmill,et al. WNT7a induces E-cadherin in lung cancer cells , 2003, Proceedings of the National Academy of Sciences of the United States of America.
[28] Vanesa Gottifredi,et al. p53 Down-Regulates CHK1 through p21 and the Retinoblastoma Protein , 2001, Molecular and Cellular Biology.
[29] Delin Chen,et al. Deacetylation of p53 modulates its effect on cell growth and apoptosis , 2000, Nature.
[30] J. Minna,et al. Allelotyping demonstrates common and distinct patterns of chromosomal loss in human lung cancer types , 1998, Genes, chromosomes & cancer.
[31] J. Minna,et al. Establishment of continuous, clonable cultures of small-cell carcinoma of lung which have amine precursor uptake and decarboxylation cell properties. , 1980, Cancer research.
[32] Barry H. Smith,et al. A continuous tumor‐cell line from a human lung carcinoma with properties of type II alveolar epithelial cells , 1976, International journal of cancer.
[33] S. Derks,et al. Epigenetic Disturbances in Colorectal Cancer , 2014 .
[34] A. Jemal,et al. Cancer statistics, 2014 , 2014, CA: a cancer journal for clinicians.
[35] Peter A. Jones,et al. Epigenetic Therapy of Cancer , 2014 .
[36] M. Maitland,et al. Carboplatin and Paclitaxel in combination with either vorinostat or placebo for first-line therapy of advanced non-small-cell lung cancer. , 2010, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.
[37] 久保 孝文. MET gene amplification or EGFR mutation activate MET in lung cancers untreated with EGFR tyrosine kinase inhibitors , 2010 .
[38] N. Dubrawsky. Cancer statistics , 2022 .