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201 results on '"Lozano, Elisa"'

6. FRI-523 Enhancing the response of cholangiocarcinoma to chemotherapy by inhibiting MRP3-mediated drug export

Author

Asensio, Maitane, primary, Briz, Oscar, additional, Herraez, Elisa, additional, Espinosa-Escudero, Ricardo A., additional, Perez-Silva, Laura, additional, Romero, Marta, additional, Temprano, Alvaro, additional, Hortelano-Hernandez, Nazaret, additional, Delgado-Calvo, Kevin, additional, Marijuan, Rebeca P., additional, Vigil, Ana Peleteiro, additional, Poetz, Oliver, additional, Efferth, Thomas, additional, Lozano, Elisa, additional, Kadioglu, Onat, additional, Marin, Jose J.G., additional, and Macias, Rocio, additional

Published
2024
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8. Liver and gastrointestinal cancers

Author

Marin, Jose J.G., primary, Macias, Rocio I.R., additional, Herraez, Elisa, additional, Lozano, Elisa, additional, Romero, Marta R., additional, Di Giacomo, Silvia, additional, Efferth, Thomas, additional, and Briz, Oscar, additional

Published
2020
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9. Contributors

Author

Alam, Camille, primary, An, Guohua, additional, Behar-Cohen, Francine, additional, Bendayan, Reina, additional, Briz, Oscar, additional, Cassoux, Nathalie, additional, Cisternino, Salvatore, additional, Declèves, Xavier, additional, Di Giacomo, Silvia, additional, Efferth, Thomas, additional, Elmquist, William F., additional, Eyal, Sara, additional, Gampa, Gautham, additional, Griffith, Jessica, additional, Hamblin, Michael R., additional, Herraez, Elisa, additional, Kim, Minjee, additional, Kumarasamy, Murali, additional, Lazarowski, Alberto, additional, Leslie, Elaine M., additional, Lozano, Elisa, additional, Macias, Rocio I.R., additional, Marin, Jose J.G., additional, Matet, Alexandre, additional, Mohammad, Afroz, additional, Morris, Marilyn E., additional, Romero, Marta R., additional, Sosnik, Alejandro, additional, Talele, Surabhi, additional, Turner, Adrian P., additional, Whitlock, Brayden D., additional, Wong, Ho-Lun, additional, and Xue, Hui-Yi, additional

Published
2020
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11. Investigation of novel hepatoblastoma chemosensitizers based on the inhibition of ABC pumps-mediated drug efflux

Author

Cives-Losada, Candela, primary, Briz, Oscar, additional, Cairo, Stefano, additional, Indersie, Emilie, additional, Efferth, Thomas, additional, Martínez-Chantar, María Luz, additional, Avila, Matías A, additional, Armengol, Carolina, additional, Lozano, Elisa, additional, Marin, Jose, additional, and Macias, Rocio Ir, additional

Published
2023
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19. Signalling networks in cholangiocarcinoma: Molecular pathogenesis, targeted therapies and drug resistance

Author

Majdi, Amine, Aoudjehane, Lynda, Ratziu, Vlad, Islam, Tawhidul, Conti, Filomena, Mestiri, Taïeb, Lagouge, Marie, Foufelle, Fabienne, Ballenghien, Florine, Ledent, Tatiana, Moldes, Marthe, Cadoret, Axelle, Delaunay, Jean-Louis, Aït-Slimane, Tounsia, Courtois, Gilles, Fève, Bruno, Scatton, Olivier, Prip-Buus, Carina, Rodrigues, Cecília M.P., Housset, Chantal, Gautheron, Jérémie, Fouassier, Laura, Marzioni, Marco, Afonso, Marta, Dooley, Steven, Gaston, Kevin, Giannelli, Gianluigi, Rodrigues, Cecilia, Lozano, Elisa, Mancarella, Serena, Segatto, Oreste, Vaquero, Javier, Marin, Jose, Coulouarn, Cédric, Centre de Recherche Saint-Antoine (CRSA), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU), Università Politecnica delle Marche [Ancona] (UNIVPM), Universidade de Lisboa = University of Lisbon (ULISBOA), Heidelberg University, University of Nottingham, UK (UON), Universidad de Salamanca, Istituti di Ricovero e Cura a Carattere Scientifico (IRCCS), Nutrition, Métabolismes et Cancer (NuMeCan), Institut National de la Recherche Agronomique (INRA)-Université de Rennes (UR)-Institut National de la Santé et de la Recherche Médicale (INSERM), LF and JV are funded by the LABEX Plas@par project and received financial state aid managed by the Agence Nationale de la Recherche, as part of the programme ‘Investissements d'avenir’ under the reference ANR-11-IDEX-0004-02. MM was funded by UNIVPM grant 040020_R.SCIENT.A_2018. CC is funded by Inserm, Univ Rennes, INCa and ITMO Cancer AVIESAN (Alliance Nationale pour les Sciences de la Vie et de la Santé) dans le cadre du Plan cancer (non-coding RNA in cancerology: fundamental to translational). KG is funded by the UK Medical Research Council (MR/N012615/1) and the Thailand Research Fund (TRF) (DBG5980005). CMPR and MBA are funded by COMPETE2020 and FCT (SAICTPAC/0019/2015 - LISBOA-01-0145-FEDER-016405), Portugal. OS is funded by AIRC (IG 16726). JJM is funded by Fondo de Investigaciones Sanitarias, Instituto de Salud Carlos III, Spain (PI16/00598, co-funded by the European Regional Development Fund/European Social Fund, ‘Investing in your future’), the Spanish Ministry of Economy, Industry and Competitiveness (SAF2016-75197-R), the Regional Government of Castile and Leon (SA063P17). The authors of this review article are members of the European Network for the Study of Cholangiocarcinoma and participate in the initiative COST Action EURO-CHOLANGIO-NET granted by the COST Association (CA18122) and Centro Internacional sobre el Envejecimiento (OLD-HEPAMARKER, 0348_CIE_6_E)., ANR-11-IDEX-0004,SUPER,Sorbonne Universités à Paris pour l'Enseignement et la Recherche(2011), Human HepCell [AP-HP Hôpital Saint-Antoine], Université Pierre et Marie Curie - Paris 6 (UPMC)-Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM)-AP-HP - Hôpital Saint-Antoine -Paris Biotech santé, Service d'Hépato-Gastroentérologie [CHU Pitié-Salpêtrière], Assistance publique - Hôpitaux de Paris (AP-HP) (APHP)-CHU Pitié-Salpêtrière [APHP], Service de chirurgie digestive hépato-bilio-pancréatique transplantation hépatique [CHU Pitié-Salpêtrière], Institut de génétique et biologie moléculaire et cellulaire (IGBMC), Université Louis Pasteur - Strasbourg I-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Centre de Recherche des Cordeliers (CRC (UMR_S 872)), Université Paris Descartes - Paris 5 (UPD5)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Centre de Recherche Saint-Antoine (CR Saint-Antoine), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Pierre et Marie Curie - Paris 6 (UPMC), Trafic Membranaire et Signalisation Dans les Cellules Epitheliales, Centre de Mathématiques Laurent Schwartz (CMLS), École polytechnique (X)-Centre National de la Recherche Scientifique (CNRS), CHU Saint-Antoine [APHP], Institut Cochin (IC UM3 (UMR 8104 / U1016)), Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Unité de Recherche sur les Maladies Cardiovasculaires, du Métabolisme et de la Nutrition = Institute of cardiometabolism and nutrition (ICAN), Assistance publique - Hôpitaux de Paris (AP-HP) (APHP)-Institut National de la Santé et de la Recherche Médicale (INSERM)-CHU Pitié-Salpêtrière [APHP]-Sorbonne Université (SU), Pathologies biliaires, fibrose et cancer du foie (Inserm UMR_S 938), Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU)-CHU Saint-Antoine [APHP], Institut National de la Santé et de la Recherche Médicale (INSERM), Department of Biochemistry, University of Bristol [Bristol], Università degli studi di Bari, iMed.UL, University of Lisbon, ITACA, Universidad Politécnica de Valencia, Université de Rennes 1 (UR1), Université de Rennes (UNIV-RENNES)-Université de Rennes (UNIV-RENNES)-Institut National de la Santé et de la Recherche Médicale (INSERM), Sorbonne Université (SU)-Institut National de la Santé et de la Recherche Médicale (INSERM)-CHU Saint-Antoine [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU), Universidade de Lisboa (ULISBOA), Institut National de Recherche pour l’Agriculture, l’Alimentation et l’Environnement (INRAE)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Rennes 1 (UR1), and Université de Rennes (UNIV-RENNES)-Université de Rennes (UNIV-RENNES)

Subjects
Drug Resistance, [SDV.CAN]Life Sciences [q-bio]/Cancer, [SDV.BC]Life Sciences [q-bio]/Cellular Biology, Computational biology, Drug resistance, Disease, Cholangiocarcinoma, 03 medical and health sciences, 0302 clinical medicine, parasitic diseases, Humans, Medicine, Molecular Targeted Therapy, Epigenetics, ComputingMilieux_MISCELLANEOUS, Hepatology, business.industry, Molecular pathogenesis, [SDV.MHEP.HEG]Life Sciences [q-bio]/Human health and pathology/Hépatology and Gastroenterology, Therapeutic resistance, 3. Good health, Bile Ducts, Intrahepatic, Signalling, Bile Duct Neoplasms, 030220 oncology & carcinogenesis, Tumour stroma, cardiovascular system, 030211 gastroenterology & hepatology, business, Signal Transduction
Abstract

Special Issue: Cholangiocarcinoma; International audience; Cholangiocarcinoma (CCA) is a deadly disease. While surgery may attain cure in a minor fraction of cases, therapeutic options in either the adjuvant or advanced setting are limited. The possibility of advancing the efficacy of therapeutic approaches to CCA relies on understanding its molecular pathogenesis and developing rational therapies aimed at interfering with oncogenic signalling networks that drive and sustain cholangiocarcinogenesis. These efforts are complicated by the intricate biology of CCA, which integrates not only the driving force of tumour cell-intrinsic alterations at the genetic and epigenetic level but also pro-tumorigenic cues conveyed to CCA cells by different cell types present in the rich tumour stroma. Herein, we review our current understanding of the mechanistic bases underpinning the activation of major oncogenic pathways causative of CCA pathogenesis. We subsequently discuss how this knowledge is being exploited to implement rationale-based and genotype-matched therapeutic approaches that predictably will radically transform CCA clinical management in the next decade. We conclude by highlighting the mechanisms of therapeutic resistance in CCA and reviewing innovative approaches to combat resistance at the preclinical and clinical level.

Published
2019
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20. Inhibition of metalloprotease hyperactivity in cystic cholangiocytes halts the development of polycystic liver diseases

Author

Urribarri, Aura D, Munoz-Garrido, Patricia, Perugorria, María J, Erice, Oihane, Merino-Azpitarte, Maite, Arbelaiz, Ander, Lozano, Elisa, Hijona, Elizabeth, Jiménez-Agüero, Raúl, Fernandez-Barrena, Maite G, Jimeno, Juan P, Marzioni, Marco, Marin, Jose J G, Masyuk, Tatyana V, LaRusso, Nicholas F, Prieto, Jesús, Bujanda, Luis, and Banales, Jesús M

Published
2014
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24. Cellular Mechanisms Accounting for the Refractoriness of Colorectal Carcinoma to Pharmacological Treatment

Author

Marin, Jose J.G., primary, Macias, Rocio I.R., additional, Monte, Maria J., additional, Herraez, Elisa, additional, Peleteiro-Vigil, Ana, additional, Blas, Beatriz Sanchez de, additional, Sanchon-Sanchez, Paula, additional, Temprano, Alvaro G., additional, Espinosa-Escudero, Ricardo A., additional, Lozano, Elisa, additional, Briz, Oscar, additional, and Romero, Marta R., additional

Published
2020
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25. Molecular Bases of Mechanisms Accounting for Drug Resistance in Gastric Adenocarcinoma

Author

Marin, Jose J. G., primary, Perez-Silva, Laura, additional, Macias, Rocio I. R., additional, Asensio, Maitane, additional, Peleteiro-Vigil, Ana, additional, Sanchez-Martin, Anabel, additional, Cives-Losada, Candela, additional, Sanchon-Sanchez, Paula, additional, Sanchez De Blas, Beatriz, additional, Herraez, Elisa, additional, Briz, Oscar, additional, and Lozano, Elisa, additional

Published
2020
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30. Signaling networks in cholangiocarcinoma: molecular pathogenesis, targeted therapies and drug resistance

Author

Fouassier, Laura, Marzioni, Marco, Afonso, Marta B., Dooley, Steven, Gaston, Kevin, Giannelli, Gianluigi, Rodrigues, Cecilia M. P., Lozano, Elisa, Mancarella, Serena, Segatto, Oreste, Vaquero, Javier, and Marin, Jose J. G.

Subjects
Hepatology, parasitic diseases, cardiovascular system
Abstract

Cholangiocarcinoma (CCA) is a deadly disease. While surgery may attain cure in a minor fraction of cases, therapeutic options in either the adjuvant or advanced setting are limited. The possibility of advancing the efficacy of therapeutic approaches to CCA relies on understanding its molecular pathogenesis and developing rational therapies aimed at interfering with oncogenic signaling networks that drive and sustain cholangiocarcinogenesis. These efforts are complicated by the intricate biology of CCA, which integrates not only the driving force of tumor?cell?intrinsic alterations at the genetic and epigenetic level, but also pro?tumorigenic cues conveyed to CCA cells by different cell types present in the rich tumor stroma. Herein, we review our current understanding of the mechanistic bases underpinning the activation of major oncogenic pathways causative of CCA pathogenesis. We subsequently discuss how this knowledge is being exploited to implement rationale?based and genotype?matched therapeutic approaches that predictably will radically transform CCA clinical management in the next decade. We conclude by highlighting mechanisms of therapeutic resistance in CCA and reviewing innovative approaches to combat resistance at the pre?clinical and clinical level.

Published
2019

31. Epigenetic events involved in organic cation transporter 1-dependent impaired response of hepatocellular carcinoma to sorafenib

Author

Al-Abdulla, Ruba, Lozano, Elisa, Macias, Rocio I R, Monte, Maria J, Briz, Oscar, O'Rourke, Colm J, Serrano, Maria A, Banales, Jesus M, Avila, Matias A, Martinez-Chantar, Maria L, Geier, Andreas, Andersen, Jesper B, Marin, Jose J G, Al-Abdulla, Ruba, Lozano, Elisa, Macias, Rocio I R, Monte, Maria J, Briz, Oscar, O'Rourke, Colm J, Serrano, Maria A, Banales, Jesus M, Avila, Matias A, Martinez-Chantar, Maria L, Geier, Andreas, Andersen, Jesper B, and Marin, Jose J G

Abstract

BACKGROUND AND PURPOSE: In hepatocellular carcinoma (HCC), the expression of the human organic cation transporter-1 (hOCT1, gene SLC22A1) is reduced. The molecular bases of this phenotypic characteristic and the relationship with the poor response of HCC to sorafenib were investigated. EXPERIMENTAL APPROACH AND KEY RESULTS: hOCT1 over-expression in human hepatoma cells (HuH7 and HepG2) enhanced sorafenib, but not regorafenib, uptake in a quinine sensitive manner. The analysis of HCC transcriptomes (TCGA, n=366) showed reduced hOCT1 mRNA, which was inversely correlated with SLC22A1 promoter methylation. The demethylating agent decitabine enhanced hOCT1 expression in hepatoma cells. In clinical samples of HCC, determination of total and alternatively spliced hOCT1 mRNA transcripts revealed enhanced proportion of aberrant short variants. Six miRNAs highly expressed in HCC (TCGA) were identified by in silico analysis as candidates to target hOCT1 mRNA. When overexpressed in HepG2 cells a significant hOCT1 mRNA decay was induced only by hsa-mir-330 and hsa-mir-1468. Analysis of 39 paired samples from TCGA revealed that only hsa-mir-330 was consistently up-regulated in HCC. The expression of the orthologues mOct1 and rOct1 was reduced in spontaneously generated HCC in Fxr-/- mice and chemically induced HCC in rats, respectively. This resulted in impaired uptake of sorafenib (HPLC-MS/MS). In mice, sorafenib treatment efficiently inhibited the growth of subcutaneously implanted tumours only if these were generated by cells over-expressing hOCT1.CONCLUSION AND IMPLICATIONS: Impaired hOCT1 expression/function in HCC, which is due in part to epigenetic modifications, plays an important role in the poor pharmacological response of this cancer to sorafenib.

Published
2019

32. Causes of hOCT1-dependent cholangiocarcinoma resistance to sorafenib and sensitization by tumor-selective gene therapy

Author

Lozano, Elisa, Macias, Rocio I R, Monte, Maria J, Asensio, Maitane, Del Carmen, Sofia, Sanchez-Vicente, Laura, Alonso-Peña, Marta, Al-Abdulla, Ruba, Munoz-Garrido, Patricia, Satriano, Letizia, O'Rourke, Colm J, Banales, Jesus M, Avila, Matias A, Martinez-Chantar, Maria L, Andersen, Jesper B, Briz, Oscar, Marin, Jose J G, Lozano, Elisa, Macias, Rocio I R, Monte, Maria J, Asensio, Maitane, Del Carmen, Sofia, Sanchez-Vicente, Laura, Alonso-Peña, Marta, Al-Abdulla, Ruba, Munoz-Garrido, Patricia, Satriano, Letizia, O'Rourke, Colm J, Banales, Jesus M, Avila, Matias A, Martinez-Chantar, Maria L, Andersen, Jesper B, Briz, Oscar, and Marin, Jose J G

Abstract

Although the multi-tyrosine kinase inhibitor, sorafenib is useful in the treatment of several cancers, cholangiocarcinoma (CCA) is refractory to this drug. Among other mechanisms of chemoresistance impaired uptake via hOCT1 (gene SLC22A1) has been suggested. Here we have investigated the events accounting for this phenotypic characteristic and have evaluated the interest of selective gene therapy strategies to overcome this limitation. Gene expression and DNA methylation of SLC22A1 were analyzed using intrahepatic (iCCA) and extrahepatic (eCCA) biopsies (Copenhagen and Salamanca cohorts; n=132) and TCGA-CHOL (n=36). Decreased hOCT1 mRNA correlated with hypermethylation status of the SLC22A1 promoter. Treatment of CCA cells with decitabine (demethylating agent) or butyrate (histone deacetylase inhibitor) restored hOCT1 expression and increased sorafenib uptake. MicroRNAs able to induce hOCT1 mRNA decay were analyzed in paired samples of TCGA-CHOL (n=9) and Copenhagen (n=57) cohorts. Consistent upregulation in tumor tissue was found for miR-141 and miR-330. High proportion of aberrant hOCT1 mRNA splicing in CCA was also seen. Lentiviral-mediated transduction of eCCA (EGI-1 and TFK-1) and iCCA (HuCCT1) cells with hOCT1 enhanced sorafenib uptake and cytotoxic effects. In chemically-induced CCA in rats reduced rOct1 expression was accompanied by impaired sorafenib uptake. In xenograft models of eCCA cells implanted in mouse liver, poor response to sorafenib was observed. However, tumor growth was markedly reduced by co-treatment with sorafenib and adenoviral vectors encoding hOCT1 under the control of the BIRC5 promoter, a gene highly upregulated in CCA. Conclusions:The reason for impaired hOCT1-mediated sorafenib uptake by CCA is multifactorial. Gene therapy capable of selectively inducing hOCT1 in tumor cells can be considered a potentially useful chemosensitization strategy to improve the response of CCA to sorafenib. This article is protected by copyright. All rig

Published
2019

33. 'Interferencias y desplazamientos. Investigación artística basada en procesos colaborativos'

Author

Marín, Eduardo, Lozano, Elisa, Escario, Patricia, Grupo de Investigación IAM-Lab (Laboratorio de Interferencias Artísticas y Mediales), Marin-Olalla, Maria Teresa, Villalonga, Rocio, Gómez, Bernabé, and Sanchez-Maldonado, Jose

Subjects
Investigación artística, Laboratorio de Interferencia Artísticas y Mediales, Arte contemporáneo, Investigación interdisciplinar, IAM-Lab
Abstract

vídeo de conferencia La coordinadora (Teresa Marín) y otros tres miembros del Laboratorio de Interferencia Artísticas y Mediales (IAM-Lab), Grupo de Investigación perteneciente a la Universidad Miguel Hernández de Elche, presentan una ponencia en la que explican la metodología de investigación artística seguida para desarrollar el proyecto "La senda es peligrosa", objeto de una muestra en la Sala de Exposiciones de la propia Facultad de Bellas Artes de Málaga, cuya inauguración tiene lugar justo después de la presente conferencia. Ésta, por tanto, sirve de introducción a la exposición, y permite que realicen un recorrido por las implicaciones que se derivan del estudio interdisciplinar en grupo. Universidad de Málaga. Campus de Excelencia Internacional Andalucía Tech.

Published
2018

35. Causes of hOCT1‐Dependent Cholangiocarcinoma Resistance to Sorafenib and Sensitization by Tumor‐Selective Gene Therapy

Author

Lozano, Elisa, primary, Macias, Rocio I.R., additional, Monte, Maria J., additional, Asensio, Maitane, additional, del Carmen, Sofia, additional, Sanchez‐Vicente, Laura, additional, Alonso‐Peña, Marta, additional, Al‐Abdulla, Ruba, additional, Munoz‐Garrido, Patricia, additional, Satriano, Letizia, additional, O'Rourke, Colm J., additional, Banales, Jesus M., additional, Avila, Matias A., additional, Martinez‐Chantar, Maria L., additional, Andersen, Jesper B., additional, Briz, Oscar, additional, and Marin, Jose J.G., additional

Published
2019
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38. Epigenetic events involved in organic cation transporter 1-dependent impaired response of hepatocellular carcinoma to sorafenib

Author

Al-Abdulla, Ruba, primary, Lozano, Elisa, additional, Macias, Rocio I R, additional, Monte, Maria J, additional, Briz, Oscar, additional, O'Rourke, Colm J, additional, Serrano, Maria A, additional, Banales, Jesus M, additional, Avila, Matias A, additional, Martinez-Chantar, Maria L, additional, Geier, Andreas, additional, Andersen, Jesper B, additional, and Marin, Jose J G, additional

Published
2019
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46. Molecular bases of the poor response of liver cancer to chemotherapy

Author

Marin, Jose J.G., primary, Briz, Oscar, additional, Herraez, Elisa, additional, Lozano, Elisa, additional, Asensio, Maitane, additional, Di Giacomo, Silvia, additional, Romero, Marta R., additional, Osorio-Padilla, Luis M., additional, Santos-Llamas, Ana I., additional, Serrano, Maria A., additional, Armengol, Carolina, additional, Efferth, Thomas, additional, and Macias, Rocio I.R., additional

Published
2018
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49. Chemoresistance and chemosensitization in cholangiocarcinoma

Author

Marin, Jose J.G., primary, Lozano, Elisa, additional, Herraez, Elisa, additional, Asensio, Maitane, additional, Di Giacomo, Silvia, additional, Romero, Marta R., additional, Briz, Oscar, additional, Serrano, Maria A., additional, Efferth, Thomas, additional, and Macias, Rocio I.R., additional

Published
2018
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