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1. Molecular Radiation Biology

Author

Reindl, Judith, Abrantes, Ana Margarida, Ahire, Vidhula, Azimzadeh, Omid, Baatout, Sarah, Baeyens, Ans, Baselet, Bjorn, Chauhan, Vinita, Da Pieve, Fabiana, Delbart, Wendy, Dobney, Caitlin Pria, Edin, Nina Frederike Jeppesen, Falk, Martin, Foray, Nicolas, François, Agnès, Frelon, Sandrine, Gaipl, Udo S., Georgakilas, Alexandros G., Guipaud, Olivier, Hausmann, Michael, Michaelidesova, Anna Jelinek, Kadhim, Munira, Marques, Inês Alexandra, Milic, Mirta, Mistry, Dhruti, Moertl, Simone, Montoro, Alegría, Obrador, Elena, Pires, Ana Salomé, Quintens, Roel, Rajan, Nicholas, Rödel, Franz, Rogan, Peter, Savu, Diana, Schettino, Giuseppe, Tabury, Kevin, Terzoudi, Georgia I., Triantopoulou, Sotiria, Viktorsson, Kristina, Wozny, Anne-Sophie, and Baatout, Sarah, editor

Published
2023
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2. Radioprotectors, Radiomitigators, and Radiosensitizers

Author

Montoro, Alegría, Obrador, Elena, Mistry, Dhruti, Forte, Giusi I., Bravatà, Valentina, Minafra, Luigi, Calvaruso, Marco, Cammarata, Francesco P., Falk, Martin, Schettino, Giuseppe, Ahire, Vidhula, Daems, Noami, Boterberg, Tom, Dainiak, Nicholas, Chaudhary, Pankaj, Baatout, Sarah, Mishra, Kaushala Prasad, and Baatout, Sarah, editor

Published
2023
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5. Oxidative stress and antioxidants in the pathophysiology of malignant melanoma

Author

Obrador, Elena, Liu-Smith, Feng, Dellinger, Ryan W, Salvador, Rosario, Meyskens, Frank L, and Estrela, José M

Subjects
Cancer, Prevention, Climate-Related Exposures and Conditions, Animals, Antioxidants, Humans, Melanoma, Oxidation-Reduction, Oxidative Stress, Signal Transduction, intracellular redox state, metastases, reactive nitrogen species, reactive oxygen species, skin cancer, tumor microenvironment, Biochemistry and Cell Biology, Biochemistry & Molecular Biology
Abstract

The high number of somatic mutations in the melanoma genome associated with cumulative ultra violet (UV) exposure has rendered it one of the most difficult of cancers to treat. With new treatment approaches based on targeted and immune therapies, drug resistance has appeared as a consistent problem. Redox biology, including reactive oxygen and nitrogen species (ROS and RNS), plays a central role in all aspects of melanoma pathophysiology, from initiation to progression and to metastatic cells. The involvement of melanin production and UV radiation in ROS/RNS generation has rendered the melanocytic lineage a unique system for studying redox biology. Overall, an elevated oxidative status has been associated with melanoma, thus much effort has been expended to prevent or treat melanoma using antioxidants which are expected to counteract oxidative stress. The consequence of this redox-rebalance seems to be two-fold: on the one hand, cells may behave less aggressively or even undergo apoptosis; on the other hand, cells may survive better after being disseminated into the circulating system or after drug treatment, thus resulting in metastasis promotion or further drug resistance. In this review we summarize the current understanding of redox signaling in melanoma at cellular and systemic levels and discuss the experimental and potential clinic use of antioxidants and new epigenetic redox modifiers.

Published
2019

8. Glioblastoma Therapy: Past, Present and Future

Author

Obrador, Elena, primary, Moreno-Murciano, Paz, additional, Oriol-Caballo, María, additional, López-Blanch, Rafael, additional, Pineda, Begoña, additional, Gutiérrez-Arroyo, Julia Lara, additional, Loras, Alba, additional, Gonzalez-Bonet, Luis G., additional, Martinez-Cadenas, Conrado, additional, Estrela, José M., additional, and Marqués-Torrejón, María Ángeles, additional

Published
2024
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11. Abstract 2826: Electromagnetic fields and hyperthermia induce lysosomal permeabilization and death in different cancer cell models: in vitro and in vivo studies

Author

Obrador, Elena, primary, Jihad-Jebbar, Ali, additional, Salvador-Palmer, Rosario, additional, López-Blanch, Rafael, additional, Oriol-Caballo, María, additional, Moreno-Murciano, María Paz, additional, Navarro, Enrique, additional, Cibrián, Rosa, additional, and Estrela, Jose M., additional

Published
2023
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18. Abstract 1390: A combination of natural polyphenols, a NAD+booster, and a Toll-like receptor 2/6 agonist exerts high radioprotection in normal tissues without interfering with the anticancer efficacy of ionizing radiations

Author

Obrador, Elena, primary, Salvador, Rosario, additional, Lopez-Blanch, Rafael, additional, Jihad-Jebbar, Ali, additional, Villaescusa, José I., additional, Montoro, Alegria, additional, Dellinger, Ryan W., additional, and Estrela, Jose M., additional

Published
2021
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21. Pterostilbene in Cancer Therapy

Author

Obrador, Elena, primary, Salvador-Palmer, Rosario, additional, Jihad-Jebbar, Ali, additional, López-Blanch, Rafael, additional, Dellinger, Thanh H., additional, Dellinger, Ryan W., additional, and Estrela, José M., additional

Published
2021
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23. Nicotinamide Riboside and Pterostilbene Cooperatively Delay Motor Neuron Failure in ALS SOD1G93A Mice

Author

Obrador, Elena, primary, Salvador, Rosario, additional, Marchio, Patricia, additional, López-Blanch, Rafael, additional, Jihad-Jebbar, Ali, additional, Rivera, Pilar, additional, Vallés, Soraya L., additional, Banacloche, Salvador, additional, Alcácer, Javier, additional, Colomer, Nuria, additional, Coronado, Javier A., additional, Alandes, Sandra, additional, Drehmer, Eraci, additional, Benlloch, María, additional, and Estrela, José M., additional

Published
2020
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26. Glutathione and Bcl-2 targeting facilitates elimination by chemoradiotherapy of human A375 melanoma xenografts overexpressing bcl-xl, bcl-2, and mcl-1

Author

Mena Salvador, Rodriguez María L, Ortega Angel, Priego Sonia, Obrador Elena, Asensi Miguel, Petschen Ignacio, Cerdá Miguel, Brown Bob D, and Estrela José M

Subjects
Medicine
Abstract

Abstract Background Bcl-2 is believed to contribute to melanoma chemoresistance. However, expression of Bcl-2 proteins may be different among melanomas. Thus correlations among expression of Bcl-2-related proteins and in vivo melanoma progression, and resistance to combination therapies, was investigated. Methods Human A375 melanoma was injected s.c. into immunodeficient nude mice. Protein expression was studied in tumor samples obtained by laser microdisection. Transfection of siRNA or ectopic overexpression were applied to manipulate proteins which are up- or down-regulated, preferentially, during melanoma progression. Anti-bcl-2 antisense oligonucleotides and chemoradiotherapy (glutathione-depleting agents, paclitaxel protein-binding particles, daunorubicin, X rays) were administered in combination. Results In vivo A375 cells down-regulated pro-apoptotic bax expression; and up-regulated anti-apoptotic bcl-2, bcl-xl, and mcl-1, however only Bcl-2 appeared critical for long-term tumor cell survival and progression in vivo. Reduction of Bcl-2, combined with partial therapies, decreased melanoma growth. But only Bcl-2 targeting plus the full combination of chemoradiotherapy eradicated A375 melanoma, and led to long-term survival (> 120 days) without recurrence in 80% of mice. Tumor regression was not due to immune stimulation. Hematology and clinical chemistry data were within accepted clinical toxicities. Conclusion Strategies to target Bcl-2, may increase the effectiveness of antitumor therapies against melanomas overexpressing Bcl-2 and likely other Bcl-2-related antiapoptotic proteins.

Published
2012
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27. Efficacy and tolerability of EH301 for amyotrophic lateral sclerosis: a randomized, double-blind, placebo-controlled human pilot study

Author

de la Rubia, JosÉ E., primary, Drehmer, Eraci, additional, Platero, JosÉ L., additional, Benlloch, MarÍa, additional, Caplliure-Llopis, Jordi, additional, Villaron-Casales, Carlos, additional, de Bernardo, Nieves, additional, AlarcÓn, Jorge, additional, Fuente, Cristian, additional, Carrera, Sandra, additional, Sancho, David, additional, GarcÍa-Pardo, Pilar, additional, Pascual, Raquel, additional, JuÁrez, Marta, additional, Cuerda-Ballester, María, additional, Forner, Alfonso, additional, Sancho-Castillo, Sandra, additional, Barrios, Carlos, additional, Obrador, Elena, additional, Marchio, Patricia, additional, Salvador, Rosario, additional, Holmes, Holly E., additional, Dellinger, Ryan W., additional, Guarente, Leonard, additional, and Estrela, José M., additional

Published
2019
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28. Changes in Chemokines and Chemokine Receptors Expression in a Mouse Model of Alzheimer's Disease

Author

Jorda, Adrián, primary, Cauli, Omar, additional, Santonja, Jose M., additional, Aldasoro, Martin, additional, Aldasoro, Constanza, additional, Obrador, Elena, additional, Vila, Jose Ma, additional, Mauricio, Ma Dolores, additional, Iradi, Antonio, additional, Guerra-Ojeda, Sol, additional, Marchio, Patricia, additional, and Valles, Soraya L., additional

Published
2019
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35. Neuronal Effects of Sugammadex in combination with Rocuronium or Vecuronium

Author

Aldasoro, Martin, primary, Jorda, Adrian, additional, Aldasoro, Constanza, additional, Marchio, Patricia, additional, Guerra-Ojeda, Sol, additional, Gimeno-Raga, Marc, additional, Mauricio, Mª Dolores, additional, Iradi, Antonio, additional, Obrador, Elena, additional, Vila, Jose Mª, additional, and Valles, Soraya L., additional

Published
2017
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36. Pterostilbene Decreases the Antioxidant Defenses of Aggressive Cancer Cells In Vivo: A Physiological Glucocorticoids- and Nrf2-Dependent Mechanism

Author

Benlloch, María, primary, Obrador, Elena, additional, Valles, Soraya L., additional, Rodriguez, María L., additional, Sirerol, J. Antoni, additional, Alcácer, Javier, additional, Pellicer, José A., additional, Salvador, Rosario, additional, Cerdá, Concha, additional, Sáez, Guillermo T., additional, and Estrela, José M., additional

Published
2016
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37. Effects of Ranolazine on Astrocytes and Neurons in Primary Culture

Author

Aldasoro, Martin, primary, Guerra-Ojeda, Sol, additional, Aguirre-Rueda, Diana, additional, Mauricio, Mª Dolores, additional, Vila, Jose Mª, additional, Marchio, Patricia, additional, Iradi, Antonio, additional, Aldasoro, Constanza, additional, Jorda, Adrian, additional, Obrador, Elena, additional, and Valles, Soraya L., additional

Published
2016
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41. Association between Pterostilbene and Quercetin Inhibits Metastatic Activity of B16 Melanoma1

Author

Ferrer, Paula, Asensi, Miguel, Segarra, Ramón, Ortega, Angel, Benlloch, María, Obrador, Elena, Varea, María T, Asensio, Gregorio, Jordá, Leonardo, and Estrela, José M

Subjects
Male, Nitrates, Liver Neoplasms, Melanoma, Experimental, Vascular Cell Adhesion Molecule-1, Hydrogen Peroxide, Integrin alpha4beta1, Mice, Inbred C57BL, Mice, Phenols, Proto-Oncogene Proteins c-bcl-2, Stilbenes, Cell Adhesion, Tumor Cells, Cultured, Animals, Quercetin, Endothelium, Vascular, Nitrites, Research Article
Abstract

Inhibition of cancer growth by resveratrol (trans-3,5,4'-trihydroxystilbene; RESV), a phytoalexin present in many plant species, is limited by its low bioavailability. Pterostilbene (3,5-dimethoxy-4'-hydroxystilbene; PTER) and quercetin (3,3',4',5,6-pentahydroxyflavone; QUER), two structurally related and naturally occurring small polyphenols, show longer half-life in vivo. In vitro growth of highly malignant B16 melanoma F10 cells (B16M-F10) is inhibited (56%) by short-time exposure (60 min/day) to PTER (40 microm) and QUER (20 microm) (approximate mean values of plasma concentrations measured within the first hour after intravenous administration of 20 mg/kg each polyphenol). Intravenous administration of PTER and QUER (20 mg/kg per day) to mice inhibits (73%) metastatic growth of B16M-F10 cell in the liver, a common site for metastasis development. The anti-metastatic mechanism involves: 1) a PTER-induced inhibition of vascular adhesion molecule 1 expression in the hepatic sinusoidal endothelium, which consequently decreases B16M-F10 cell adhesion to the endothelium through very late activation antigen 4; and 2) a QUER- and PTER-induced inhibition of Bcl-2 expression in metastatic cells, which sensitizes them to vascular endothelium-induced cytotoxicity. Our findings demonstrate that the association of PTER and QUER inhibits metastatic melanoma growth and extends host survival.

Published
2005

42. Glucocorticoid Receptor Knockdown Decreases the Antioxidant Protection of B16 Melanoma Cells: An Endocrine System-Related Mechanism that Compromises Metastatic Cell Resistance to Vascular Endothelium-Induced Tumor Cytotoxicity

Author

Obrador, Elena, primary, Valles, Soraya L., additional, Benlloch, María, additional, Sirerol, J. Antoni, additional, Pellicer, José A., additional, Alcácer, Javier, additional, Coronado, Javier Alcácer-F., additional, and Estrela, José M., additional

Published
2014
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43. Stress hormones promote growth of B16-F10 melanoma metastases: an interleukin 6-and glutathione-dependent mechanism

Author

Universitat Politècnica de València. Instituto de Reconocimiento Molecular y Desarrollo Tecnológico - Institut de Reconeixement Molecular i Desenvolupament Tecnològic, Ministerio de Ciencia e Innovación, Valles, Soraya L., Benlloch, Maria, Rodriguez , María Lucía, Mena-Mollá, Salvador, Pellicer, Jose A, Asensi-Miralles, Miguel Ángel, Obrador, Elena, Estrela, José María, Universitat Politècnica de València. Instituto de Reconocimiento Molecular y Desarrollo Tecnológico - Institut de Reconeixement Molecular i Desenvolupament Tecnològic, Ministerio de Ciencia e Innovación, Valles, Soraya L., Benlloch, Maria, Rodriguez , María Lucía, Mena-Mollá, Salvador, Pellicer, Jose A, Asensi-Miralles, Miguel Ángel, Obrador, Elena, and Estrela, José María

Abstract

[EN] Background: Interleukin (IL)-6 (mainly of tumor origin) activates glutathione (GSH) release from hepatocytes and its interorgan transport to B16-F10 melanoma metastatic foci. We studied if this capacity to overproduce IL-6 is regulated by cancer cell-independent mechanisms. Methods: Murine B16-F10 melanoma cells were cultured, transfected with red fluorescent protein, injected i.v. into syngenic C57BL/6J mice to generate lung and liver metastases, and isolated from metastatic foci using high-performance cell sorting. Stress hormones and IL-6 levels were measured by ELISA, and CRH expression in the brain by in situ hybridization. DNA binding activity of NF-kappa B, CREB, AP-1, and NF-IL-6 was measured using specific transcription factor assay kits. IL-6 expression was measured by RT-PCR, and silencing was achieved by transfection of anti-IL-6 small interfering RNA. GSH was determined by HPLC. Cell death analysis was distinguished using fluorescence microscopy, TUNEL labeling, and flow cytometry techniques. Statistical analyses were performed using Student's t test. Results: Plasma levels of stress-related hormones (adrenocorticotropin hormone, corticosterone, and noradrenaline) increased, following a circadian pattern and as compared to non-tumor controls, in mice bearing B16-F10 lung or liver metastases. Corticosterone and noradrenaline, at pathophysiological levels, increased expression and secretion of IL-6 in B16-F10 cells in vitro. Corticosterone- and noradrenaline-induced transcriptional up-regulation of IL-6 gene involves changes in the DNA binding activity of nuclear factor-kappa B, cAMP response element-binding protein, activator protein-1, and nuclear factor for IL-6. In vivo inoculation of B16-F10 cells transfected with anti-IL-6-siRNA, treatment with a glucocorticoid receptor blocker (RU-486) or with a beta-adrenoceptor blocker (propranolol), increased hepatic GSH whereas decreased plasma IL-6 levels and metastatic growth. Corticosterone, but not NOR

Published
2013

44. Glutathione and Bcl-2 targeting facilitates elimination by chemoradiotherapy of human A375 melanoma xenografts overexpressing bcl-xl, bcl-2, and mcl-1

Author

Universitat Politècnica de València. Instituto de Reconocimiento Molecular y Desarrollo Tecnológico - Institut de Reconeixement Molecular i Desenvolupament Tecnològic, Ministerio de Ciencia e Innovación, Mena-Mollá, Salvador, Rodríguez, Maria L., Ortega, Ángel, Priego, Sonia, Obrador, Elena, Asensi, Miguel, Petschen, Ignacio, Cerda, Miguel, Brown, Bob D., Estrela, Jose M., Universitat Politècnica de València. Instituto de Reconocimiento Molecular y Desarrollo Tecnológico - Institut de Reconeixement Molecular i Desenvolupament Tecnològic, Ministerio de Ciencia e Innovación, Mena-Mollá, Salvador, Rodríguez, Maria L., Ortega, Ángel, Priego, Sonia, Obrador, Elena, Asensi, Miguel, Petschen, Ignacio, Cerda, Miguel, Brown, Bob D., and Estrela, Jose M.

Abstract

[EN] Background: Bcl-2 is believed to contribute to melanoma chemoresistance. However, expression of Bcl-2 proteins may be different among melanomas. Thus correlations among expression of Bcl-2-related proteins and in vivo melanoma progression, and resistance to combination therapies, was investigated. Methods: Human A375 melanoma was injected s.c. into immunodeficient nude mice. Protein expression was studied in tumor samples obtained by laser microdisection. Transfection of siRNA or ectopic overexpression were applied to manipulate proteins which are up- or down-regulated, preferentially, during melanoma progression. Anti-bcl-2 antisense oligonucleotides and chemoradiotherapy (glutathione-depleting agents, paclitaxel protein-binding particles, daunorubicin, X rays) were administered in combination. Results: In vivo A375 cells down-regulated pro-apoptotic bax expression; and up-regulated anti-apoptotic bcl-2, bcl-xl, and mcl-1, however only Bcl-2 appeared critical for long-term tumor cell survival and progression in vivo. Reduction of Bcl-2, combined with partial therapies, decreased melanoma growth. But only Bcl-2 targeting plus the full combination of chemoradiotherapy eradicated A375 melanoma, and led to long-term survival (> 120 days) without recurrence in 80% of mice. Tumor regression was not due to immune stimulation. Hematology and clinical chemistry data were within accepted clinical toxicities. Conclusion: Strategies to target Bcl-2, may increase the effectiveness of antitumor therapies against melanomas overexpressing Bcl-2 and likely other Bcl-2-related antiapoptotic proteins.

Published
2012

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