Search Results - "Gruber, Franz X"

Dynamical models of mutated chronic myelogenous leukemia cells for a post-imatinib treatment scenario: Response to dasatinib or nilotinib therapy by Woywod, Clemens, Gruber, Franz X, Engh, Richard A, Flå, Tor

“…Targeted inhibition of the oncogenic BCR-ABL1 fusion protein using the ABL1 tyrosine kinase inhibitor imatinib has become standard therapy for chronic…”
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Data driven polypharmacological drug design for lung cancer: analyses for targeting ALK, MET, and EGFR by Narayanan, Dilip, Gani, Osman A. B. S. M., Gruber, Franz X. E., Engh, Richard A.

“…Drug design of protein kinase inhibitors is now greatly enabled by thousands of publicly available X-ray structures, extensive ligand binding data, and…”
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The quantitative level of T315I mutated BCR-ABL predicts for major molecular response to second-line nilotinib or dasatinib treatment in patients with chronic myeloid leukemia by Lange, Thoralf, Ernst, Thomas, Gruber, Franz X, Maier, Jacqueline, Cross, Michael, Müller, Martin C, Niederwieser, Dietger, Hochhaus, Andreas, Pfirrmann, Markus

“…The BCR-ABL T315I mutation causes resistance to imatinib, nilotinib and dasatinib in chronic myeloid leukemia. Forty BCR-ABL positive patients with imatinib…”
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Discontinuation of tyrosine kinase inhibitor therapy in chronic myeloid leukaemia (EURO-SKI): a prespecified interim analysis of a prospective, multicentre, non-randomised, trial by Saussele, Susanne, Richter, Johan, Guilhot, Joelle, Gruber, Franz X, Hjorth-Hansen, Henrik, Almeida, Antonio, Janssen, Jeroen J W M, Mayer, Jiri, Koskenvesa, Perttu, Panayiotidis, Panayiotis, Olsson-Strömberg, Ulla, Martinez-Lopez, Joaquin, Rousselot, Philippe, Vestergaard, Hanne, Ehrencrona, Hans, Kairisto, Veli, Machová Poláková, Katerina, Müller, Martin C, Mustjoki, Satu, Berger, Marc G, Fabarius, Alice, Hofmann, Wolf-Karsten, Hochhaus, Andreas, Pfirrmann, Markus, Mahon, Francois-Xavier, Ossenkoppele, Gert, Pagoni, Maria N., Söderlund, Stina, Escoffre-Barbe, Martine, Etienne, Gabriel, Dengler, Jolanta, Huguet, Francoise, von Bubnoff, Nikolas, Klamova, Hana, Faber, Edgar, Guilhot, Francois, Lotfi, Kourosh, Rea, Delphine, Brümmendorf, Tim H., de Greef, Gorgine E., Stenke, Leif, Nicolini, Franck E., Legros, Laurence, Burchert, Andreas, Voglova, Jaroslava, Charbonnier, Aude, Gyan, Emmanuel, Kunzmann, Volker, Westerweel, Peter E.

“…Tyrosine kinase inhibitors (TKIs) have improved the survival of patients with chronic myeloid leukaemia. Many patients have deep molecular responses, a…”
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A co-operative evaluation of different methods of detecting BCR-ABL kinase domain mutations in patients with chronic myeloid leukemia on second-line dasatinib or nilotinib therapy after failure of imatinib by Ernst, Thomas, Gruber, Franz X, Pelz-Ackermann, Oliver, Maier, Jacqueline, Pfirrmann, Markus, Muller, Martin C, Mikkola, Ingvild, Porkka, Kimmo, Niederwieser, Dietger, Hochhaus, Andreas, Lange, Thoralf

“…1 III. Medizinische Klinik, Universitätsmedizin Mannheim, Universität Heidelberg, Mannheim, Germany 2 Institute of Pharmacy, University of Tromsø, Tromsø,…”
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Detection of Drug-Resistant Clones in Chronic Myelogenous Leukemia Patients during Dasatinib and Nilotinib Treatment by Gruber, Franz X, Ernst, Thomas, Kiselev, Yuri, Hochhaus, Andreas, Mikkola, Ingvild

“…Imatinib effectively inhibits the tyrosine kinase activity conferred by the BCR-ABL gene [fusion gene of BCR (breakpoint cluster region) and ABL1 (c-abl…”
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Intracellular and Surface Distribution of Monocyte Tissue Factor: Application to Intersubject Variability by Egorina, Elena M, Sovershaev, Mikhail A, Bjørkøy, Geir, Gruber, Franz X.E, Olsen, Jan O, Parhami-Seren, Behnaz, Mann, Kenneth G, Østerud, Bjarne

“…OBJECTIVE—The high and low responder phenomenon describes individual differences in lipopolysaccharide (LPS)-induced monocyte tissue factor (TF) activity. We…”
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The role of TFPI in regulation of TF-induced thrombogenicity on the surface of human monocytes by Basavaraj, Manjunath Goolyam, Gruber, Franz X, Sovershaev, Mikhail, Appelbom, Hege I, Østerud, Bjarne, Petersen, Lars C, Hansen, John-Bjarne

“…Abstract Introduction Although the procoagulant reactivity of monocytes largely depends on expression and cell surface presentation of tissue factor (TF),…”
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Circulating monocytes mirror the imbalance in TF and TFPI expression in carotid atherosclerotic plaques with lipid-rich and calcified morphology by Basavaraj, Manjunath Goolyam, Sovershaev, Mikhail A, Egorina, Elena M, Gruber, Franz X, Bogdanov, Vladimir Y, Fallon, John T, Østerud, Bjarne, Mathiesen, Ellisiv B, Hansen, John-Bjarne

“…Abstract Background Thrombogenicity of atherosclerotic plaque largely depends on plaque morphology and their content of tissue factor (TF) and tissue factor…”
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BCR-ABL isoforms associated with intrinsic or acquired resistance to imatinib: more heterogeneous than just ABL kinase domain point mutations? by Gruber, Franz X., Lundán, Tuija, Goll, Rasmus, Silye, Aleksandra, Mikkola, Ingvild, Rekvig, Ole Petter, Knuutila, Sakari, Remes, Kari, Gedde-Dahl, Tobias, Porkka, Kimmo, Hjorth-Hansen, Henrik

“…Imatinib, a small molecule inhibitor of ABL, PDGFR and C-KIT, has revolutionized treatment of chronic myeloid leukaemia (CML). However, resistance to treatment…”
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Chronic myelogenous leukemia with the e6a2 BCR-ABL and lacking imatinib response: presentation of two cases by Vefring, Hege K, Gruber, Franz X E, Wee, Line, Hovland, Randi, Hjorth-Hansen, Henrik, Gedde Dahl, Tobias, Meyer, Peter

“…The BCR-ABL fusion gene represents the hallmark of chronic myelogenous leukemia (CML) and is derived from a translocation between chromosome 9 and 22. The…”
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Dynamical models of mutated chronic myelogenous leukemia cells for a postimatinib treatment scenario: Response to dasatinib or nilotinib therapy by Woywod, Clemens Joachim, Gruber, Franz, Engh, Richard Alan, Flå, Tor

“…Targeted inhibition of the oncogenic BCR-ABL1 fusion protein using the ABL1 tyrosine kinase inhibitor imatinib has become standard therapy for chronic…”
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Effects of Dasatinib and Interferon-α Combination Treatment on the Immune System in CML by Ilander, Mette, Lähteenmäki, Hanna, Olsson-Stromberg, Ulla, Stentoft, Jesper, Richter, Johan, Koskenvesa, Perttu, Höglund, Martin, Dreimane, Arta, Porkka, Kimmo, Gedde-Dahl, Tobias, Gjertsen, Björn T., Gruber, Franz X., Stenke, Leif, Myhr-Eriksson, Kristina, Markevärn, Berit, Lubking, Anna, Vestergaard, Hanne, Udby, Lene, Weis Bjerrum, Ole, Hjorth-Hansen, Henrik, Mustjoki, Satu

“…Background: In chronic myeloid leukemia (CML) the combination treatment of tyrosine kinase inhibitors (TKIs) with interferon-α (IFN-α) has proved to be…”
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Safety and Efficacy of Addition of Pegylated Interferon alpha2b to Standard Dose Dasatinib in Newly Diagnosed Chronic Phase CML Patients by Hjorth-Hansen, Henrik, Stentoft, Jesper, Richter, Johan, Koskenvesa, Perttu, Dreimane, Arta, Porkka, Kimmo, Gedde-Dahl, Tobias, Gjertsen, Bjorn, Gruber, Franz X., Hoglund, Martin, Lubking, Anna, Myhr-Eriksson, Kristina, Markevärn, Berit, Vestergaard, Hanne, Weis Bjerrum, Ole, Stenke, Leif, Mustjoki, Satu, Stromberg, Ulla

“…▪ Rationale: Dasatinib (DAS) and interferon have different modes of action and may have synergistic activity in CML, due to both antineoplastic and…”
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A novel Bcr-Abl splice isoform is associated with the L248V mutation in CML patients with acquired resistance to imatinib by Gruber, F X, Hjorth-Hansen, H, Mikkola, I, Stenke, L, Johansen, T

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Kinetics of BCR-ABL Mutant Clones Determines Resistance in CML on Second Generation TKI Treatment by Gruber, Franz X, Ernst, Thomas, Maier, Jaqueline, Müller, Martin C., Mikkola, Ingvild, Porkka, Kimmo, Niederwieser, Dietger, Hochhaus, Andreas, Lange, Thoralf

“…BCR-ABL kinase domain (KD) mutations are the major mechanism of acquired imatinib resistance in patients (pts) with chronic myeloid leukemia (CML). Second…”
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Extracellular Signal-Regulated Protein Kinase 5 Mediates Resistance of Human Chronic Myeloid Leukemia K562 Cells to Imatinib by Sovershaev, Mikhail A., Egorina, Elena M., Gruber, Franz X., Bjørkøy, Geir, Johansen, Terje

“…Mutations in the Abl kinase domain and Bcr-Abl gene amplification have been recognised as the most common mechanisms of resistance to Imatinib (Gleevec) in…”
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