The pan-HDAC inhibitor panobinostat acts as a sensitizer for erlotinib activity in EGFR-mutated and -wildtype non-small cell lung cancer cells

[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 .