Search Results - "V Mansat-De Mas"

Oncogenic FLT3-ITD supports autophagy via ATF4 in acute myeloid leukemia by Heydt, Q, Larrue, C, Saland, E, Bertoli, S, Sarry, J-E, Besson, A, Manenti, S, Joffre, C, Mansat-De Mas, V

“…In acute myeloid leukemia (AML), internal tandem duplication mutations in the FLT3 tyrosine kinase receptor (FLT3-ITD) account for up to 25% of cases and are…”
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Impact of TET2 mutations on response rate to azacitidine in myelodysplastic syndromes and low blast count acute myeloid leukemias by Itzykson, R, Kosmider, O, Cluzeau, T, Mansat-De Mas, V, Dreyfus, F, Beyne-Rauzy, O, Quesnel, B, Vey, N, Gelsi-Boyer, V, Raynaud, S, Preudhomme, C, Adès, L, Fenaux, P, Fontenay, M

“…The impact of ten-eleven-translocation 2 (TET2) mutations on response to azacitidine (AZA) in MDS has not been reported. We sequenced the TET2 gene in 86 MDS…”
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RET fusion genes are associated with chronic myelomonocytic leukemia and enhance monocytic differentiation by Ballerini, P, Struski, S, Cresson, C, Prade, N, Toujani, S, Deswarte, C, Dobbelstein, S, Petit, A, Lapillonne, H, Gautier, E-F, Demur, C, Lippert, E, Pages, P, Mansat- De Mas, V, Donadieu, J, Huguet, F, Dastugue, N, Broccardo, C, Perot, C, Delabesse, E

“…Myeloproliferative neoplasms are frequently associated with aberrant constitutive tyrosine kinase (TK) activity resulting from chimaeric fusion genes or point…”
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Cutaneous mastocytosis in adults with a serum tryptase level < 20 ng mL–1: why we should investigate further by Jendoubi, F., Shourick, J., Negretto, M., Laurent, C., Apoil, P.A., Evrard, S., Mansat‐De Mas, V., Severino‐Freire, M., Mailhol, C., Degboé, Y., Dubreuil, P., Hermine, O., Paul, C., Bulai Livideanu, C.

“…Dear Editor, Mastocytosis is a rare disease characterized by the accumulation/proliferation of abnormal mast cells (MCs).1 Mastocytosis is categorized into…”
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A crosstalk between the Wnt and the adhesion-dependent signaling pathways governs the chemosensitivity of acute myeloid leukemia by DE TONI, F, RACAUD-SULTAN, C, MANENTI, S, YSEBAERT, L, CHICANNE, G, MANSAT-DE MAS, V, CARIVEN, C, MESANGE, F, SALLES, J.-P, DEMUR, C, ALLOUCHE, M, PAYRASTRE, B

“…Relapses following chemotherapy are a major hindrance to patients' survival in acute myeloid leukemia (AML). To investigate the role of the hematopoietic niche…”
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Human telomerase is regulated by erythropoietin and transforming growth factor-β in human erythroid progenitor cells by PRADE-HOUDELLIER, N, FREBET, E, BEYNE-RAUZY, O, DEMUR, C, GAUTIER, E.-F, DELHOMMEAU, F, BENNACEUR -GRISCELLI, A.-L, GAUDIN, C, MARTINEL, V, LAURENT, G, MANSAT-DE MAS, V

“…Telomerase catalytic subunit (hTERT) exerts important cellular functions including telomere homeostasis, genetic stability, cell survival and perhaps…”
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Expression of β-catenin by acute myeloid leukemia cells predicts enhanced clonogenic capacities and poor prognosis by YSEBAERT, L, CHICANNE, G, MANENTI, S, RACAUD-SULTAN, C, DEMUR, C, DE TONI, F, PRADE-HOUDELLIER, N, RUIDAVETS, J.-B, MANSAT-DE MAS, V, RIGAL-HUGUET, F, LAURENT, G, PAYRASTRE, B

“…Activation of the Wnt/beta-catenin pathway has recently been shown to be crucial to the establishment of leukemic stem cells in chronic myeloid leukemia. We…”
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Pim kinases phosphorylate Chk1 and regulate its functions in acute myeloid leukemia by Yuan, L L, Green, A S, Bertoli, S, Grimal, F, Mansat-De Mas, V, Dozier, C, Tamburini, J, Récher, C, Didier, C, Manenti, S

“…Phosphorylation by Akt on Ser 280 was reported to induce cytoplasmic retention and inactivation of CHK1 with consequent genetic instability in PTEN−/− cells…”
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The short form of RON is expressed in acute myeloid leukemia and sensitizes leukemic cells to cMET inhibitors by Fialin, C, Larrue, C, Vergez, F, Sarry, J E, Bertoli, S, Mansat-De Mas, V, Demur, C, Delabesse, E, Payrastre, B, Manenti, S, Roche, S, Récher, C

“…Several receptor tyrosine kinases (TKs) are involved in the pathogenesis of acute myeloid leukemia (AML). Here, we have assessed the expression of the…”
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P477: PHENOTYPICALLY‐DEFINED STAGES OF LEUKEMIA ARREST PREDICT MAIN DRIVER MUTATIONS SUBGROUPS, AND OUTCOME IN ACUTE MYELOID LEUKEMIA by Vergez, F., Largeaud, L., Bertoli, S., Nicolau‐Travers, M.‐L., Rieu, J.‐B., Vergnolle, I., Saland, E., Sarry, A., Tavitian, S., Huguet, F., Picard, M., Vial, J.‐P., Lechevalier, N., Bidet, A., Dumas, P.‐Y., Pigneux, A., Luquet, I., Mansat‐De Mas, V., Delabesse, E., Carroll, M., Danet‐Desnoyers, G., Sarry, J.‐E., Recher, C.

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TNFα stimulates NKG2D-mediated lytic activity of acute myeloid leukemic cells by GUILLOTON, F, DE THONEL, A, JEAN, C, DEMUR, C, MANSAT-DE MAS, V, LAURENT, G, QUILLET-MARY, A

“…The mechanism by which leukemic cells interfere with normal hematopoiesis remains unclear. We show here that, whereas the leukemic KG1a cells are naturally…”
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306 Impact of TET2 mutations on response rate to azacitidine in myelodysplastic syndromes and low blast count acute myeloid leukemias by Kosmider, O, Itzykson, R, Cluzeau, T, Mansat-De Mas, V, Dreyfus, F, Beyne-Rauzy, O, Quesnel, B, Vey, N, Gelsi-Boyer, V, Raynaud, S, Preudhomme, C, Ades, L, Fenaux, P, Fontenay, M

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305 TET2 and IDH1/2 mutations in secondary acute myeloid leukemias: A French retrospective study by Kosmider, O, Mansat-De Mas, V, Delabesse, E, Cornillet-lefevre, P, Blanchet, O, Récher, C, Grabar, S, Raynaud, S, Lacombe, C, Bernard, O, Ifrah, N, Dreyfus, F, Fontenay, M

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C020 Prevalence of TET2 mutations in MDS by Kosmider, O, Gelsi-Boyer, V, Cheok, M, Grabar, S, Guardiola, P, Beyne-Rauzy, O, Quesnel, B, Solary, E, Vey, N, Hunault-Berger, M, Fenaux, P, Mansat-de Mas, V, Guesnu, M, Viguie, F, Lacombe, C, Vainchenker, W, Preudhomme, C, Birnbaum, D, Dreyfus, F, Bernard, O, Fontenay, M

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Oxidative stress‐induced activation of Lyn recruits sphingomyelinase and is requisite for its stimulation by Ara‐C by Bezombes, Christine, Plo, Isabelle, Mas, Véronique Mansat-De, Quillet-Mary, Anne, Nègre-Salvayre, Anne, Laurent, Guy, Jaffrézou, Jean-Pierre

“…ABSTRACT Induction of apoptosis is considered to be the underlying mechanism that accounts for the efficiency of chemotherapeutic drugs. The identification of…”
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Implication of radical oxygen species in ceramide generation, c-Jun N-terminal kinase activation and apoptosis induced by daunorubicin by Mansat-de Mas, V, Bezombes, C, Quillet-Mary, A, Bettaïeb, A, D'orgeix, A D, Laurent, G, Jaffrézou, J P

“…Anthracyclines such as daunorubicin (DNR) generate radical oxygen species (ROS), which account, at least in part, for their cytotoxic effect. We observed that…”
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The phosphoinositide 3-kinase/Akt pathway is activated by daunorubicin in human acute myeloid leukemia cell lines by Plo, I., Bettaïeb, A., Payrastre, B., Mansat-De Mas, V., Bordier, C., Rousse, A., Kowalski-Chauvel, A., Laurent, G., Lautier, D.

“…Daunorubicin induces apoptosis in myeloid leukemia cells by activation of neutral sphingomyelinase and ceramide generation occurring 4–10 min after…”
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Daunorubicin- and mitoxantrone-triggered phosphatidylcholine hydrolysis: implication in drug-induced ceramide generation and apoptosis by Bettaïeb, A, Plo, I, Mansat-De Mas, V, Quillet-Mary, A, Levade, T, Laurent, G, Jaffrézou, J P

“…Several studies have suggested that diacylglycerol can affect the induction of apoptosis induced by toxicants and ceramide. The present study demonstrates that…”
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Cutaneous mastocytosis in adult patients with serum tryptase level under 20 ng/ml: why we should investigate further by Jendoubi, F, Shourick, J, Negretto, M, Laurent, C, Apoil, P A, Evrard, S, Mansat-De Mas, V, Severino-Freire, M, Mailhol, C, Degboé, Y, Dubreuil, P, Hermine, O, Paul, C, Bulai Livideanu, C

“…Mastocytosis is a rare disease characterized by the accumulation/proliferation of abnormal mast cells (MC) [1]. Mastocytosis is categorized into isolated…”
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Tumor necrosis factor alpha induces senescence and chromosomal instability in human leukemic cells by BEYNE-RAUZY, Odile, RECHER, Christian, DASTUGUE, Nicole, DEMUR, Cécile, POTTIER, Géraldine, LAURENT, Guy, SABATIER, Laure, MANSAT-DE MAS, Véronique

“…Previous studies have documented that Tumor necrosis factor alpha (TNFalpha) is a potent negative regulator of normal hematopoiesis. However, the mechanism by…”
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