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<publisher>HAL CCSD</publisher>
<title lang=en>Mycophenolic Acid overcomes imatinib and nilotinib resistance of chronic myeloid leukemia cells by apoptosis or a senescent-like cell cycle arrest.</title>
<creator>Drullion, Claire</creator>
<creator>Lagarde, Valérie</creator>
<creator>Gioia, Romain</creator>
<creator>Legembre, Patrick</creator>
<creator>Priault, Muriel</creator>
<creator>Cardinaud, Bruno</creator>
<creator>Lippert, Eric</creator>
<creator>Mahon, François-Xavier</creator>
<creator>Pasquet, Jean-Max</creator>
<contributor>Biothérapies des maladies génétiques et cancers ; Université Bordeaux Segalen - Bordeaux 2 - Institut National de la Santé et de la Recherche Médicale (INSERM)</contributor>
<contributor>Récepteur de mort et échappement tumoral ; Institut de recherche, santé, environnement et travail [Rennes] (Irset) ; Université d'Angers (UA) - Université des Antilles et de la Guyane (UAG) - Université de Rennes 1 (UR1) - École des Hautes Études en Santé Publique [EHESP] (EHESP) - Institut National de la Santé et de la Recherche Médicale (INSERM) - Structure Fédérative de Recherche en Biologie et Santé de Rennes ( Biosit : Biologie - Santé - Innovation Technologique ) - Université d'Angers (UA) - Université des Antilles et de la Guyane (UAG) - Université de Rennes 1 (UR1) - École des Hautes Études en Santé Publique [EHESP] (EHESP) - Institut National de la Santé et de la Recherche Médicale (INSERM) - Structure Fédérative de Recherche en Biologie et Santé de Rennes ( Biosit : Biologie - Santé - Innovation Technologique )</contributor>
<contributor>Institut de biochimie et génétique cellulaires (IBGC) ; Université Bordeaux Segalen - Bordeaux 2 - Centre National de la Recherche Scientifique (CNRS)</contributor>
<contributor>Ligue Nationale Contre le Cancer Comité de la Dordogne- l'Université Victor Ségalen Bordeaux 2 - la région Aquitaine - l'Institut National de la Santé et de la Recherche Médicale.</contributor>
<description>International audience</description>
<source>Leukemia Research and Treatment</source>
<identifier>hal-00846103</identifier>
<identifier>https://hal.archives-ouvertes.fr/hal-00846103</identifier>
<identifier>https://hal.archives-ouvertes.fr/hal-00846103/document</identifier>
<identifier>https://hal.archives-ouvertes.fr/hal-00846103/file/Mycophenolic_Acid_Overcomes-accepted.pdf</identifier>
<source>https://hal.archives-ouvertes.fr/hal-00846103</source>
<source>Leukemia Research and Treatment, 2012, 2012, pp.861301. 〈10.1155/2012/861301〉</source>
<identifier>PUBMED : 23213550</identifier>
<relation>info:eu-repo/semantics/altIdentifier/pmid/23213550</relation>
<identifier>DOI : 10.1155/2012/861301</identifier>
<relation>info:eu-repo/semantics/altIdentifier/doi/10.1155/2012/861301</relation>
<language>en</language>
<subject>[SDV.BC] Life Sciences [q-bio]/Cellular Biology</subject>
<type>info:eu-repo/semantics/article</type>
<type>Journal articles</type>
<description lang=en>We used K562 cells sensitive or generated resistant to imatinib or nilotinib to investigate their response to mycophenolic acid (MPA). MPA induced DNA damage leading to cell death with a minor contribution of apoptosis, as revealed by annexin V labeling (up to 25%). In contrast, cell cycle arrest and positive staining for senescence-associated β-galactosidase activity were detected for a large cell population (80%). MPA-induced cell death was potentialized by the inhibition of autophagy and this is associated to the upregulation of apoptosis. In contrast, senescence was neither decreased nor abrogated in autophagy deficient K562 cells. Primary CD34 cells from CML patients sensitive or resistant to imatinib or nilotinib respond to MPA although apoptosis is mainly detected. These results show that MPA is an interesting tool to overcome resistance in vitro and in vivo mainly in the evolved phase of the disease.</description>
<date>2012</date>
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