Search

Your search keyword '"Zouhour Neffati"' showing total 2 results
Start Over Author "Zouhour Neffati" Language english
2 results on '"Zouhour Neffati"'

1. Iron chelation: an adjuvant therapy to target metabolism, growth and survival of murine PTEN-deficient T lymphoma and human T lymphoblastic leukemia/lymphoma

Author

Emmanuel Griessinger, Zouhour Neffati, Nicolas Sirvent, Alexandra Popa, Célia Rosilio, Marielle Nebout, Véronique Imbert, Jean-François Peyron, Vera Heimeroth, Didier Mary, Joy Benadiba, Centre méditérannéen de médecine moléculaire ( C3M ), Université Nice Sophia Antipolis ( UNS ), Université Côte d'Azur ( UCA ) -Université Côte d'Azur ( UCA ) -Institut National de la Santé et de la Recherche Médicale ( INSERM ), Université Nice Sophia Antipolis - Faculté de Médecine ( UNS UFR Médecine ), Université Côte d'Azur ( UCA ) -Université Côte d'Azur ( UCA ), CHU Nice, Institut de pharmacologie moléculaire et cellulaire ( IPMC ), Université Côte d'Azur ( UCA ) -Université Côte d'Azur ( UCA ) -Centre National de la Recherche Scientifique ( CNRS ), Centre Hospitalier Régional Universitaire [Montpellier] ( CHRU Montpellier ), Centre méditerranéen de médecine moléculaire (C3M), Université Nice Sophia Antipolis (... - 2019) (UNS), COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-Université Côte d'Azur (UCA)-Institut National de la Santé et de la Recherche Médicale (INSERM), Université Nice Sophia Antipolis - Faculté de Médecine (UNS UFR Médecine), COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-COMUE Université Côte d'Azur (2015-2019) (COMUE UCA), Centre Hospitalier Universitaire de Nice (CHU Nice), Institut de pharmacologie moléculaire et cellulaire (IPMC), Centre National de la Recherche Scientifique (CNRS)-Université Nice Sophia Antipolis (... - 2019) (UNS), COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-Université Côte d'Azur (UCA), and Centre Hospitalier Régional Universitaire [Montpellier] (CHRU Montpellier)

Subjects
0301 basic medicine, Cancer Research, Gene Expression, synergy, Apoptosis, Pharmacology, Precursor T-Cell Lymphoblastic Leukemia-Lymphoma, chemotherapy, [ SDV.CAN ] Life Sciences [q-bio]/Cancer, T-lymphoblastic leukemia/lymphoma, Mice, 0302 clinical medicine, hemic and lymphatic diseases, [ SDV.MHEP.HEM ] Life Sciences [q-bio]/Human health and pathology/Hematology, Cells, Cultured, chemistry.chemical_classification, leukemia, Drug Synergism, [SDV.MHEP.HEM]Life Sciences [q-bio]/Human health and pathology/Hematology, Hematology, Iron metabolism, 3. Good health, Deferoxamine, Leukemia, Oncology, Chemotherapy, Adjuvant, 030220 oncology & carcinogenesis, addiction, medicine.drug, DNA damage, DNA repair, Cell Survival, Iron, Transferrin receptor, [SDV.CAN]Life Sciences [q-bio]/Cancer, Biology, Iron Chelating Agents, Lymphoma, T-Cell, 03 medical and health sciences, Antigens, CD, Cell Line, Tumor, Receptors, Transferrin, medicine, Animals, Asparaginase, Humans, Doxorubicin, PTEN Phosphohydrolase, medicine.disease, Disease Models, Animal, 030104 developmental biology, chemistry, Transferrin, Reactive Oxygen Species, DNA Damage
Abstract

International audience; Iron is an essential nutrient, acting as a catalyst for metabolic reactions that are fundamental to cell survival and proliferation. Iron complexed to transferrin is delivered to the metabolism after endocytosis via the CD71 surface receptor. We found that transformed cells from a murine PTEN-deficient T-cell lymphoma model and from T-cell acute lymphoblastic leukemia/lymphoma (T-ALL/T-LL) cell lines overexpress CD71. As a consequence, the cells developed an addiction toward iron whose chelation by deferoxamine (DFO) dramatically affected their survival to induce apoptosis. Interestingly, DFO displayed synergistic activity with three ALL-specific drugs: dexamethasone, doxorubicin, and L-asparaginase. DFO appeared to act through a reactive oxygen species-dependent DNA damage response and potentiated the action of an inhibitor of the PARP pathway of DNA repair. Our results demonstrate that targeting iron metabolism could be an interesting adjuvant therapy for acute lymphoblastic leukemia.

Published
2017
Full Text
View/download PDF

2. Pharmacological inhibition of carbonic anhydrase XII interferes with cell proliferation and induces cell apoptosis in T-cell lymphomas

Author

Didier Mary, Véronique Imbert, Zouhour Neffati, Emmanuel Griessinger, Thijs J. Hagenbeek, Johanna Chiche, Marielle Nebout, Vahid Asnafi, Sally-Ann Poulsen, Célia Rosilio, Claudiu T. Supuran, Nadia Lounnas, Hergen Spits, Jean-François Peyron, Slama, Catherine, Cytokines, hématopoïèse et réponse immune (CHRI), Université Paris Descartes - Paris 5 (UPD5) - Institut National de la Santé et de la Recherche Médicale (INSERM) - Centre National de la Recherche Scientifique (CNRS), Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Amsterdam institute for Infection and Immunity, Amsterdam Gastroenterology Endocrinology Metabolism, and Tytgat Institute for Liver and Intestinal Research

Subjects
Gene isoform, Cancer Research, T cell, Apoptosis, Lymphoma, T-Cell, 03 medical and health sciences, Mice, 0302 clinical medicine, Downregulation and upregulation, Carbonic anhydrase, hemic and lymphatic diseases, Cell Line, Tumor, medicine, T-cell lymphoma, Animals, Humans, Carbonic Anhydrase Inhibitors, ComputingMilieux_MISCELLANEOUS, 030304 developmental biology, Carbonic Anhydrases, Cell Proliferation, 0303 health sciences, biology, Cell growth, PTEN Phosphohydrolase, Hydrogen-Ion Concentration, medicine.disease, 3. Good health, Cell biology, Lymphoma, medicine.anatomical_structure, Oncology, 030220 oncology & carcinogenesis, biology.protein, Cancer research
Abstract

The membrane-bound carbonic anhydrase isoforms CAIX and CAXII, underpin a pH-regulating system that enables hypoxic tumor cell survival. Here, we observed for the first time an upregulation of CAXII in T-cell acute lymphoblastic leukemia/lymphoma (T-ALL/LL) cells. First we showed that CAXII is overexpressed in thymocytes from tPTEN−/− mice suffering of T lymphoma and that its pharmacological inhibition decreased cell proliferation and induced apoptosis. The same results were observed with the SupT1 human T cell lymphoma line. In addition we observed an upregulation of CAXII in human T-ALL samples supporting the case that CAXII may represent a new therapeutic target for T-ALL/LL.

Published
2013

Catalog

Books, media, physical & digital resources
See catalog results