Blar i forfatter Artikler, rapporter og annet (kjemi) "Gruber, Franz"

Viser treff 1-3 av 3

    • Data driven polypharmacological drug design for lung cancer: analyses for targeting ALK, MET, and EGFR 

      Narayanan, Dilip; Gani, Osman; Gruber, Franz; Engh, Richard Alan (Journal article; Tidsskriftartikkel; Peer reviewed, 2017-07-04)
      Drug design of protein kinase inhibitors is now greatly enabled by thousands of publicly available X-ray structures, extensive ligand binding data, and optimized scaffolds coming off patent. The extensive data begin to enable design against a spectrum of targets (polypharmacology); however, the data also reveal heterogeneities of structure, subtleties of chemical interactions, and apparent inconsistencies ...

    • Dynamical models of mutated chronic myelogenous leukemia cells for a postimatinib treatment scenario: Response to dasatinib or nilotinib therapy 

      Woywod, Clemens Joachim; Gruber, Franz; Engh, Richard Alan; Flå, Tor (Journal article; Tidsskriftartikkel; Peer reviewed, 2017-07-05)
      Targeted inhibition of the oncogenic BCR-ABL1 fusion protein using the ABL1 tyrosine kinase inhibitor imatinib has become standard therapy for chronic myelogenous leukemia (CML), with most patients reaching total and durable remission. However, a significant fraction of patients develop resistance, commonly due to mutated ABL1 kinase domains. This motivated development of second-generation drugs ...

    • 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 

      Lange, Thoralf; Ernst, Thomas; Gruber, Franz; Maier, Jacqueline; Cross, Michael; Müller, Martin C.; Niederwieser, Dietger; Hochhaus, Andreas; Pfirrmann, Markus (Journal article; Tidsskriftartikkel; Peer reviewed, 2013-05)
      The BCR-ABL T315I mutation causes resistance to imatinib, nilotinib and dasatinib in chronic myeloid leukemia. Forty BCR-ABL positive patients with imatinib resistance were analyzed for T315I mutated clones after six months on nilotinib or dasatinib treatment by quantitative allele-specific ligation polymerase chain reaction with a sensitivity of 0.05%. Ligation polymerase chain reaction revealed ...