Nikolas von Bubnoff

Summary

Affiliation: Klinikum rechts der Isar
Country: Germany

Publications

  1. pmc Chronic myelogenous leukemia: treatment and monitoring
    Nikolas von Bubnoff
    Medizinische Klinik und Poliklinik, Klinikum rechts der Isar, Technische Universitat Munchen, Germany
    Dtsch Arztebl Int 107:114-21. 2010
  2. doi request reprint FMS-like tyrosine kinase 3-internal tandem duplication tyrosine kinase inhibitors display a nonoverlapping profile of resistance mutations in vitro
    Nikolas von Bubnoff
    III Medizinische Klinik, Klinikum rechts der Isar, Technische Universitat Munchen, Munchen, Germany
    Cancer Res 69:3032-41. 2009
  3. ncbi request reprint [An alternative Abl-kinase inhibitor overcomes imatinib resistance mutations of Bcr-Abl oncogenes]
    N von Bubnoff
    III Medizinische Klinik und Poliklinik, Klinikum rechts der Isar der Technischen Universitat Munchen
    Dtsch Med Wochenschr 129:2100-3. 2004
  4. doi request reprint The low frequency of clinical resistance to PDGFR inhibitors in myeloid neoplasms with abnormalities of PDGFRA might be related to the limited repertoire of possible PDGFRA kinase domain mutations in vitro
    N von Bubnoff
    III Medizinische Klinik und Poliklinik, Klinikum rechts der Isar, Technische Universitat Munchen, Munchen, Germany
    Oncogene 30:933-43. 2011
  5. ncbi request reprint A cell-based screening strategy that predicts mutations in oncogenic tyrosine kinases: implications for clinical resistance in targeted cancer treatment
    Nikolas von Bubnoff
    Department of Internal Medicine III, Technical University of Munich, Munich, Germany
    Cell Cycle 4:400-6. 2005
  6. ncbi request reprint Bcr-Abl resistance screening predicts a limited spectrum of point mutations to be associated with clinical resistance to the Abl kinase inhibitor nilotinib (AMN107)
    Nikolas von Bubnoff
    Department of Internal Medicine III, Technical University of Munich, D 81675 Munich, Germany
    Blood 108:1328-33. 2006
  7. pmc Anti-CD20 B-cell depletion enhances monocyte reactivity in neuroimmunological disorders
    Klaus Lehmann-Horn
    Department of Neurology, Technische Universitat Munchen, Munich, Germany
    J Neuroinflammation 8:146. 2011
  8. ncbi request reprint A cell-based screen for resistance of Bcr-Abl-positive leukemia identifies the mutation pattern for PD166326, an alternative Abl kinase inhibitor
    Nikolas von Bubnoff
    Department of Internal Medicine III, Technical University of Munich, D 81675 Munich, Germany
    Blood 105:1652-9. 2005
  9. doi request reprint Imatinib and leptomycin B are effective in overcoming imatinib-resistance due to Bcr-Abl amplification and clonal evolution but not due to Bcr-Abl kinase domain mutation
    Rama Krishna Kancha
    Dept of Internal Medicine III, Technical University of Munich, Ismaningerstr 22, 81675 Munich, Germany
    Haematologica 93:1718-22. 2008
  10. ncbi request reprint Inhibition of wild-type and mutant Bcr-Abl by pyrido-pyrimidine-type small molecule kinase inhibitors
    Nikolas von Bubnoff
    Department of Internal Medicine III, Technical University of Munich, Trogerstrasse 32, D 81675 Munich, Germany
    Cancer Res 63:6395-404. 2003

Collaborators

Detail Information

Publications17

  1. pmc Chronic myelogenous leukemia: treatment and monitoring
    Nikolas von Bubnoff
    Medizinische Klinik und Poliklinik, Klinikum rechts der Isar, Technische Universitat Munchen, Germany
    Dtsch Arztebl Int 107:114-21. 2010
    ..The tyrosine kinase inhibitor imatinib was approved for the treatment of CML in 2002. Data from clinical trials allow a comparison of treatment options...
  2. doi request reprint FMS-like tyrosine kinase 3-internal tandem duplication tyrosine kinase inhibitors display a nonoverlapping profile of resistance mutations in vitro
    Nikolas von Bubnoff
    III Medizinische Klinik, Klinikum rechts der Isar, Technische Universitat Munchen, Munchen, Germany
    Cancer Res 69:3032-41. 2009
    ..Therefore, combinations of FLT3 inhibitors may be useful to prevent FLT3 resistance mutations in the setting of FLT3-ITD-positive AML...
  3. ncbi request reprint [An alternative Abl-kinase inhibitor overcomes imatinib resistance mutations of Bcr-Abl oncogenes]
    N von Bubnoff
    III Medizinische Klinik und Poliklinik, Klinikum rechts der Isar der Technischen Universitat Munchen
    Dtsch Med Wochenschr 129:2100-3. 2004
    ..We aimed to examine, whether the alternative Abl Kinaseinhibitor SKI-DV 2 - 43 may be capable of suppressing the growth of cells expressing mutant forms of Bcr-Abl...
  4. doi request reprint The low frequency of clinical resistance to PDGFR inhibitors in myeloid neoplasms with abnormalities of PDGFRA might be related to the limited repertoire of possible PDGFRA kinase domain mutations in vitro
    N von Bubnoff
    III Medizinische Klinik und Poliklinik, Klinikum rechts der Isar, Technische Universitat Munchen, Munchen, Germany
    Oncogene 30:933-43. 2011
    ..In addition, these findings would help to select the appropriate second-line drug in cases of imatinib-resistant disease and may be translated to other neoplasms driven by activated forms of PDGFR-A or -B...
  5. ncbi request reprint A cell-based screening strategy that predicts mutations in oncogenic tyrosine kinases: implications for clinical resistance in targeted cancer treatment
    Nikolas von Bubnoff
    Department of Internal Medicine III, Technical University of Munich, Munich, Germany
    Cell Cycle 4:400-6. 2005
    ..We here provide a detailed methodological description, and discuss the implications of this strategy for different clinically relevant oncogenic tyrosine kinases...
  6. ncbi request reprint Bcr-Abl resistance screening predicts a limited spectrum of point mutations to be associated with clinical resistance to the Abl kinase inhibitor nilotinib (AMN107)
    Nikolas von Bubnoff
    Department of Internal Medicine III, Technical University of Munich, D 81675 Munich, Germany
    Blood 108:1328-33. 2006
    ..However, our study indicates that clinical resistance to nilotinib may be associated with the predominant emergence of T315I...
  7. pmc Anti-CD20 B-cell depletion enhances monocyte reactivity in neuroimmunological disorders
    Klaus Lehmann-Horn
    Department of Neurology, Technische Universitat Munchen, Munich, Germany
    J Neuroinflammation 8:146. 2011
    ..We elucidated the regulatory role of un-activated B-cells in EAE and investigated whether anti-CD20 may collaterally diminish regulatory B-cell properties in treatment of neuroimmunological disorders...
  8. ncbi request reprint A cell-based screen for resistance of Bcr-Abl-positive leukemia identifies the mutation pattern for PD166326, an alternative Abl kinase inhibitor
    Nikolas von Bubnoff
    Department of Internal Medicine III, Technical University of Munich, D 81675 Munich, Germany
    Blood 105:1652-9. 2005
    ..Thus, this robust and simple screening system provides a rational basis for combinatorial and sequential treatment strategies in targeted cancer therapy...
  9. doi request reprint Imatinib and leptomycin B are effective in overcoming imatinib-resistance due to Bcr-Abl amplification and clonal evolution but not due to Bcr-Abl kinase domain mutation
    Rama Krishna Kancha
    Dept of Internal Medicine III, Technical University of Munich, Ismaningerstr 22, 81675 Munich, Germany
    Haematologica 93:1718-22. 2008
    ..Thus, a partial inhibition of Bcr-Abl by imatinib is required for this approach in agreement with the proposed mode of action...
  10. ncbi request reprint Inhibition of wild-type and mutant Bcr-Abl by pyrido-pyrimidine-type small molecule kinase inhibitors
    Nikolas von Bubnoff
    Department of Internal Medicine III, Technical University of Munich, Trogerstrasse 32, D 81675 Munich, Germany
    Cancer Res 63:6395-404. 2003
    ....
  11. doi request reprint Sequential inhibitor therapy in CML: in vitro simulation elucidates the pattern of resistance mutations after second- and third-line treatment
    Robert C Bauer
    III Medizinische Klinik und Poliklinik, Klinikum rechts der Isar, Technische Universitat Munchen, Munchen, Germany
    Clin Cancer Res 19:2962-72. 2013
    ..We aimed at modeling sequential tyrosine kinase inhibitor (TKI) resistance in vitro to compare the sequences imatinib-nilotinib-dasatinib and imatinib-dasatinib-nilotinib...
  12. ncbi request reprint BCR-ABL gene mutations in relation to clinical resistance of Philadelphia-chromosome-positive leukaemia to STI571: a prospective study
    Nikolas von Bubnoff
    Department of Internal Medicine III, Laboratory of Leukemogenesis, Technical University of Munich, Ismaningerstrasse 22, 81675, Munich, Germany
    Lancet 359:487-91. 2002
    ..However, most patients with advanced disease relapse despite continued treatment with STI571. We aimed to find out whether point mutations in BCR-ABL cause resistance to STI571...
  13. pmc Differential sensitivity of ERBB2 kinase domain mutations towards lapatinib
    Rama Krishna Kancha
    Department of Internal Medicine III, Technical University of Munich, Munich, Germany
    PLoS ONE 6:e26760. 2011
    ..However, the sensitivity of lapatinib towards clinically observed ERBB2 mutations is not known...
  14. doi request reprint Oncologist's/haematologist's view on the roles of pathologists for molecular targeted cancer therapy
    Ulrich Keller
    III Medical Department, Technische Universitat Munchen, Munich, Germany
    J Cell Mol Med 14:805-17. 2010
    ..After all, the success of a molecular targeted therapy is clearly determined by the significance of the targeted structure for the biology of cancer and the ability of the malignant cell to evade specific inhibition...
  15. doi request reprint Functional analysis of epidermal growth factor receptor (EGFR) mutations and potential implications for EGFR targeted therapy
    Rama Krishna Kancha
    Department of Internal Medicine III, Technical University of Munich, Munich, Germany
    Clin Cancer Res 15:460-7. 2009
    ..Thus, we aimed to characterize a comprehensive panel of clinically observed EGFR mutations...
  16. pmc Aurora kinases A and B are up-regulated by Myc and are essential for maintenance of the malignant state
    Jürgen den Hollander
    III Medical Department, Technische Universitat Munchen, Munich, Germany
    Blood 116:1498-505. 2010
    ..Importantly, apoptosis provoked by Aurk inhibition was p53 independent, suggesting that Aurka/Aurkb inhibitors will show efficacy in treating primary or relapsed malignancies having Myc involvement and/or loss of p53 function...
  17. ncbi request reprint Endothelial-like cells expanded from CD34+ blood cells improve left ventricular function after experimental myocardial infarction
    Ilka Ott
    I Department of Medicine, Technical University Munich, Munich, Germany
    FASEB J 19:992-4. 2005
    ..Therefore, in vitro expanded EPC-derived endothelial cells may be beneficial in the treatment of ischemic disease...