Sequence-dependent enhancement of paclitaxel toxicity in non–small cell lung cancer by 17-allylamino 17-demethoxygeldanamycin Dao M. Nguyen, MD, FRCSC,

Slides:

Advertisements

Similar presentations

The selective epidermal growth factor receptor tyrosine kinase inhibitor PD suppresses expression of prometastasis phenotypes in malignant pleural.

Advertisements

Enhancement of depsipeptide-mediated apoptosis of lung or esophageal cancer cells by flavopiridol: Activation of the mitochondria-dependent death-signaling.

Antiproliferative and apoptotic effects of rofecoxib on esophageal cancer in vitro1 Linda Vona-Davis, Ph.D., Dale R Riggs, Barbara J Jackson, David W.

Manish R. Patel, DO, Blake A

Protective Function of p27KIP1 against Apoptosis in Small Cell Lung Cancer Cells in Unfavorable Microenvironments Akira Masuda, Hirotaka Osada, Yasushi.

Astragaloside IV Enhances Cisplatin Chemosensitivity in Non-Small Cell Lung Cancer Cells Through Inhibition of B7-H3 Cell Physiol Biochem 2016;40:

Vascular endothelial growth factor expression in non-small-cell lung cancer: Prognostic significance in squamous cell carcinoma Hideyuki Imoto, MD, Toshihiro.

Induction of apoptosis of lung and esophageal cancer cells treated with the combination of histone deacetylase inhibitor (trichostatin A) and protein.

Therapy-Resistant Cancer Stem Cells Have Differing Sensitivity to Photon versus Proton Beam Radiation Xiaochun Zhang, MD, Steven H. Lin, MD, PhD, Bingliang.

Lost in translation The Journal of Thoracic and Cardiovascular Surgery

The Autophagy Inhibitor Chloroquine Overcomes the Innate Resistance of Wild-Type EGFR Non-Small-Cell Lung Cancer Cells to Erlotinib Yiyu Zou, PhD, Yi-He.

Inactivation of Both FHIT and p53 Cooperate in Deregulating Proliferation-Related Pathways in Lung Cancer Francesca Andriani, PharmD, Elena Roz, MD,

Manish R. Patel, DO, Blake A

Enhancement of paclitaxel-mediated cytotoxicity in lung cancer cells by 17-allylamino geldanamycin: in vitro and in vivo analysis Dao M Nguyen, MD, Dominique.

Gossypol, a phytochemical with BH3-mimetic property, sensitizes cultured thoracic cancer cells to Apo2 ligand/tumor necrosis factor–related apoptosis-inducing.

Therapy-Resistant Cancer Stem Cells Have Differing Sensitivity to Photon versus Proton Beam Radiation Xiaochun Zhang, MD, Steven H. Lin, MD, PhD, Bingliang.

Combined treatment with cisplatin and sirolimus to enhance cell death in human mesothelioma Mor-Li Hartman, PhD, John Matthew Esposito, BA, Beow Yong.

A High Content Clonogenic Survival Drug Screen Identifies MEK Inhibitors as Potent Radiation Sensitizers for KRAS Mutant Non–Small-Cell Lung Cancer Steven.

Characterization of Aurora A and Its Impact on the Effect of Cisplatin-Based Chemotherapy in Patients with Non–Small Cell Lung Cancer Peng Kuang, Zuhua.

Depletion of DNA methyltransferase 1 and/or DNA methyltransferase 3b mediates growth arrest and apoptosis in lung and esophageal cancer and malignant.

Resistance to EGFR-TKI Can Be Mediated through Multiple Signaling Pathways Converging upon Cap-Dependent Translation in EGFR-Wild Type NSCLC Manish R.

Keloid Fibroblasts Resist Ceramide-Induced Apoptosis by Overexpression of Insulin- Like Growth Factor I Receptor Hiroshi Ishihara, Hiroshi Yoshimoto,

Volume 191, Issue 1, Pages (January 2014)

Thomas A. d‘Amato, MD, PhD, Rodney J

Marissa V. Powers, Paul A. Clarke, Paul Workman Cancer Cell

A Histone Deacetylase Inhibitor LBH589 Downregulates XIAP in Mesothelioma Cell Lines Which is Likely Responsible for Increased Apoptosis With TRAIL James.

Enhancement of depsipeptide-mediated apoptosis of lung or esophageal cancer cells by flavopiridol: Activation of the mitochondria-dependent death-signaling.

Targeting of the Hedgehog signal transduction pathway suppresses survival of malignant pleural mesothelioma cells in vitro Min You, PhD, Javier Varona-Santos,

Induction of apoptosis of lung and esophageal cancer cells treated with the combination of histone deacetylase inhibitor (trichostatin A) and protein.

MET Increases the Sensitivity of Gefitinib-Resistant Cells to SN-38, an Active Metabolite of Irinotecan, by Up-Regulating the Topoisomerase I Activity

Potentiation of paclitaxel cytotoxicity in lung and esophageal cancer cells by pharmacologic inhibition of the phosphoinositide 3-kinase/protein kinase.

Marissa V. Powers, Paul A. Clarke, Paul Workman Cancer Cell

Inhibition of phosphatidylinositol 3-kinase/Akt and histone deacetylase activity induces apoptosis in non–small cell lung cancer in vitro and in vivo

The Autophagy Inhibitor Chloroquine Overcomes the Innate Resistance of Wild-Type EGFR Non-Small-Cell Lung Cancer Cells to Erlotinib Yiyu Zou, PhD, Yi-He.

Ground glass opacity of the lung: The veil that needs lifting

Induction of apoptosis in malignant pleural mesothelioma cells by activation of the Fas (Apo-1/CD95) death-signal pathway John H. Stewart, MD, Dao M.

Pharmacokinetics of paclitaxel administered by hyperthermic retrograde isolated lung perfusion techniques David S. Schrump, MDa, Suoping Zhai, PhDb,

Combination of Gefitinib and Pemetrexed Prevents the Acquisition of TKI Resistance in NSCLC Cell Lines Carrying EGFR-Activating Mutation Silvia La Monica,

Enhancement of Apo2L/TRAIL (tumor necrosis factor–related apoptosis-inducing ligand)–induced apoptosis in non–small cell lung cancer cell lines by chemotherapeutic.

James L. Cox, MD, Niv Ad, MD, Terry Palazzo, RN, MS

Induction of MAGE-3 expression in lung and esophageal cancer cells

Clusterin Regulates Drug-Resistance in Melanoma Cells

AT-101, a Pan-Bcl-2 Inhibitor, Leads to Radiosensitization of Non-small Cell Lung Cancer Luigi Moretti, MD, Bo Li, MD, Kwang Woon Kim, PhD, Heidi Chen,

Gene therapy for lung cancer: Enhancement of tumor suppression by a combination of sequential systemic cisplatin and adenovirus-mediated p53 gene transfer

Lobe-specific extent of systematic lymph node dissection for non–small cell lung carcinomas according to a retrospective study of metastasis and prognosis

The Human Immunodeficiency Virus Protease Inhibitor Ritonavir Inhibits Lung Cancer Cells, in Part, by Inhibition of Survivin Anjaiah Srirangam, PhD,

Lovastatin Sensitizes Lung Cancer Cells to Ionizing Radiation: Modulation of Molecular Pathways of Radioresistance and Tumor Suppression Toran Sanli,

Shigeyuki Sasaki, MD, PhD (by invitation), James D

BV6, an IAP Antagonist, Activates Apoptosis and Enhances Radiosensitization of Non- small Cell Lung Carcinoma In Vitro Wenyan Li, MD, PhD, Bo Li, MD,

Downregulated ABCG2 Enhances Sensitivity to Topoisomerase I Inhibitor in Epidermal Growth Factor Receptor Tyrosine Kinase Inhibitor-Resistant Non-small.

Chadrick E Denlinger, MD, Michael D Keller, BS, Marty W Mayo, PhD, R

The selective epidermal growth factor receptor tyrosine kinase inhibitor PD suppresses expression of prometastasis phenotypes in malignant pleural.

Is tissue the issue? Brian E. Louie, MD, MHA, MPH, FRCSC, FACS

Yang Zhang, MD, Haiquan Chen, MD, PhD

Support Your Specialty

Histone Deacetylase Inhibitor Romidepsin Enhances Anti-Tumor Effect of Erlotinib in Non-small Cell Lung Cancer (NSCLC) Cell Lines Wei Zhang, PhD, Michael.

Schedule-Dependent Interaction between the Proteosome Inhibitor Bortezomib and the EGFR-TK Inhibitor Erlotinib in Human Non-small Cell Lung Cancer Cell.

Chadrick E. Denlinger, MD, Brian K. Rundall, DO, Michael D

Differential Regulation of Cyclooxygenase-2 Expression by Phytosphingosine Derivatives, NAPS and TAPS, and its Role in the NAPS or TAPS-Mediated Apoptosis

MET Increases the Sensitivity of Gefitinib-Resistant Cells to SN-38, an Active Metabolite of Irinotecan, by Up-Regulating the Topoisomerase I Activity

Gefitinib Enhances Cytotoxicities of Antimicrotubule Agents in Non–Small-Cell Lung Cancer Cells Exhibiting No Sensitizing Epidermal Growth Factor Receptor.

Cisplatin enhances apoptosis induced by a tumor-selective adenovirus expressing tumor necrosis factor–related apoptosis-inducing ligand Rishindra M.

Carcinoma of the esophagus: Prognostic significance of histologic type

Who is your plastic surgeon

Harald Renz, MD, Chaya Brodie, PhD, Katherine Bradley, BS, Donald Y. M

Linda W. Martin, MD, MPH, FCCP, FACS, Gail E

Robert J. Cerfolio, MD, FACS, FCCP, Ayesha S. Bryant, MSPH, MD

Aritoshi Hattori, MD, Kenji Suzuki, MD

Samuel Kim, MD The Journal of Thoracic and Cardiovascular Surgery

The tp53 genotype but not immunohistochemical result is predictive of response to cisplatin-based neoadjuvant therapy in stage III non–small cell lung.

Presentation transcript:

Sequence-dependent enhancement of paclitaxel toxicity in non–small cell lung cancer by 17-allylamino 17-demethoxygeldanamycin Dao M. Nguyen, MD, FRCSC, Aaron Chen, MS, Arnold Mixon, BS, David S. Schrump, MD, FACS The Journal of Thoracic and Cardiovascular Surgery Volume 118, Issue 5, Pages 908-915 (November 1999) DOI: 10.1016/S0022-5223(99)70061-9 Copyright © 1999 Mosby, Inc. Terms and Conditions

Fig. 1 Constitutive expression of p185 oncoprotein and its depletion by 17-AAGA in NSCLC cells. Normal human bronchial epithelial cells (NHBE) as well as H460 and H1299 cells express low levels of p185. Other cell lines overexpress this oncoprotein (15- to 31-fold higher than level detected in normal human bronchial epithelial cells). Exposure to either 20 nmol/L or 80 nmol/L 17-AAGA for 24 hours resulted in dose-dependent reduction of p185 in all cell lines tested. Data are mean ± SD for 3 independent experiments. The Journal of Thoracic and Cardiovascular Surgery 1999 118, 908-915DOI: (10.1016/S0022-5223(99)70061-9) Copyright © 1999 Mosby, Inc. Terms and Conditions

Fig. 2 Dose-dependent growth inhibition of NSCLC in vitro by 17-AAGA. Cells were seeded in 96-well flat-bottom microtiter plates and, after overnight incubation, continuously exposed to varying doses of 17-AAGA for 96 hours. Viable cells were quantitated by MTT assay. IC50 values, estimated from dose-response curves, are indicated in parentheses. Data are mean ± SD for 3 independent experiments. The Journal of Thoracic and Cardiovascular Surgery 1999 118, 908-915DOI: (10.1016/S0022-5223(99)70061-9) Copyright © 1999 Mosby, Inc. Terms and Conditions

Fig. 3 A, Representative dose-response curves of H661 (high p185) and H1299 (low p185) cells treated with paclitaxel (Taxol) alone or concurrently with either 20 nmol/L or 40 nmol/L 17-AAGA (schedule A combination). Data are mean ± SD for 4 independent experiments. B, Reduction of paclitaxel (Taxol) IC50 values by 17-AAGA in NSCLC cells expressing high levels of p185 (P = .001, P < .0001, P < .0001, P < .0001 for H358, H322, H661, and H522 cells, respectively, by 1-way analysis of variance). Data are mean ± SD for 4 independent experiments. Right upper corner graph indicates multiplicity of reduction of paclitaxel IC50 values (indicating enhanced paclitaxel sensitivity) in cells treated with paclitaxel and either 20 nmol/L or 40 nmol/L 17-AAGA. The Journal of Thoracic and Cardiovascular Surgery 1999 118, 908-915DOI: (10.1016/S0022-5223(99)70061-9) Copyright © 1999 Mosby, Inc. Terms and Conditions

Fig. 4 A, Representative dose-response curves of H661 (high p185) and H1299 (low p185) cells treated with paclitaxel (Taxol, Tx) or schedule B drug combination. Exposure of cells to 17-AAGA for 24 hours before paclitaxel and 17-AAGA treatment induced paclitaxel resistance, as indicated by higher fractions of viable cells and translated into elevation of paclitaxel IC50 values. Data are mean ± SD for 4 independent experiments. B, Significant elevation of paclitaxel IC50 values (indicating decreased paclitaxel sensitivity) by schedule B drug combination in 5 cell lines studied (2 low p185 and 3 high p185 cell lines). The Journal of Thoracic and Cardiovascular Surgery 1999 118, 908-915DOI: (10.1016/S0022-5223(99)70061-9) Copyright © 1999 Mosby, Inc. Terms and Conditions

Fig. 5 Time-course of induction of cell cycle arrest at G1 phase by 17-AAGA treatment in H1299, H661, and H358 (P = .42 and P < .0001 [asterisk], P = .01 and P = .03 [number sign], and P = .19 and P = .0001 [double asterisk] for 17-AAGA treatment versus control at 24 hours and 48 hours, respectively, by the Student t test). Data are mean ± SD for 3 independent experiments. The Journal of Thoracic and Cardiovascular Surgery 1999 118, 908-915DOI: (10.1016/S0022-5223(99)70061-9) Copyright © 1999 Mosby, Inc. Terms and Conditions

Fig. 6 Significant induction of apoptosis in H322 and H661 cells treated for 60 hours with schedule A combination (paclitaxel [Taxol] at 50 nmol/L and 500 nmol/L and 17-AAGA at 40 nmol/L). Control preparations were cells treated either with 17-AAGA or with paclitaxel (P = .0001 [asterisk], P = .0008 [number sign], P = .001 [double asterisk], and P = .0001 [double number sign] for schedule A combination versus paclitaxel alone by Student t test. Data are mean ± SD for 3 independent experiments. The Journal of Thoracic and Cardiovascular Surgery 1999 118, 908-915DOI: (10.1016/S0022-5223(99)70061-9) Copyright © 1999 Mosby, Inc. Terms and Conditions