Stephan Mathas

Summary

Country: Germany

Publications

  1. ncbi Inhibition of NF-kappaB essentially contributes to arsenic-induced apoptosis
    Stephan Mathas
    Max Delbruck Center for Molecular Medicine, FG Dörken, Robert Rossle Str 10, D 13125 Berlin, Germany
    Blood 102:1028-34. 2003
  2. ncbi Elevated NF-kappaB p50 complex formation and Bcl-3 expression in classical Hodgkin, anaplastic large-cell, and other peripheral T-cell lymphomas
    Stephan Mathas
    Max Delbruck Center for Molecular Medicine, FG Dörken, D 13125 Berlin, Germany
    Blood 106:4287-93. 2005
  3. pmc c-FLIP mediates resistance of Hodgkin/Reed-Sternberg cells to death receptor-induced apoptosis
    Stephan Mathas
    Max Delbruck Center for Molecular Medicine, FG Dörken, D 13125 Berlin, Germany
    J Exp Med 199:1041-52. 2004
  4. doi Aberrant expression of the Th2 cytokine IL-21 in Hodgkin lymphoma cells regulates STAT3 signaling and attracts Treg cells via regulation of MIP-3alpha
    Björn Lamprecht
    Max Delbruck Center for Molecular Medicine, Berlin, Germany
    Blood 112:3339-47. 2008
  5. ncbi Classical Hodgkin lymphoma is characterized by high constitutive expression of activating transcription factor 3 (ATF3), which promotes viability of Hodgkin/Reed-Sternberg cells
    Martin Janz
    Hematology, Oncology, and Tumorimmunology, Max Delbruck Center for Molecular Medicine, Robert Rossle Str 10, 13092 Berlin, Germany
    Blood 107:2536-9. 2006
  6. ncbi Intrinsic inhibition of transcription factor E2A by HLH proteins ABF-1 and Id2 mediates reprogramming of neoplastic B cells in Hodgkin lymphoma
    Stephan Mathas
    Max Delbruck Center for Molecular Medicine, 13125 Berlin, Germany
    Nat Immunol 7:207-15. 2006
  7. pmc Nuclear factor kappaB-dependent gene expression profiling of Hodgkin's disease tumor cells, pathogenetic significance, and link to constitutive signal transducer and activator of transcription 5a activity
    Michael Hinz
    Max Delbruck Center for Molecular Medicine, 13125 Berlin, Germany
    J Exp Med 196:605-17. 2002
  8. ncbi Reprogramming of B lymphoid cells in human lymphoma pathogenesis
    Martin Janz
    Max Delbruck Center for Molecular Medicine, Berlin, Germany
    Cell Cycle 5:1057-61. 2006
  9. ncbi The pathogenesis of classical Hodgkin's lymphoma: a model for B-cell plasticity
    Stephan Mathas
    Max Delbruck Center for Molecular Medicine, Robert Rossle Str 10, 13125 Berlin, Germany
    Hematol Oncol Clin North Am 21:787-804. 2007
  10. pmc Gene deregulation and spatial genome reorganization near breakpoints prior to formation of translocations in anaplastic large cell lymphoma
    Stephan Mathas
    Max Delbruck Center for Molecular Medicine, Robert Rossle Strasse 10, 13125 Berlin, Germany
    Proc Natl Acad Sci U S A 106:5831-6. 2009

Collaborators

Detail Information

Publications20

  1. ncbi Inhibition of NF-kappaB essentially contributes to arsenic-induced apoptosis
    Stephan Mathas
    Max Delbruck Center for Molecular Medicine, FG Dörken, Robert Rossle Str 10, D 13125 Berlin, Germany
    Blood 102:1028-34. 2003
    ..We conclude that inhibition of NF-kappaB contributes to arsenic-induced apoptosis. Furthermore, pharmacologic inhibition of the IKK/NF-kappaB activity might be a powerful treatment option for Hodgkin lymphoma...
  2. ncbi Elevated NF-kappaB p50 complex formation and Bcl-3 expression in classical Hodgkin, anaplastic large-cell, and other peripheral T-cell lymphomas
    Stephan Mathas
    Max Delbruck Center for Molecular Medicine, FG Dörken, D 13125 Berlin, Germany
    Blood 106:4287-93. 2005
    ..Together, these data suggest that elevated Bcl-3 expression has an important function in cHL and peripheral T-NHL, in particular ALCL...
  3. pmc c-FLIP mediates resistance of Hodgkin/Reed-Sternberg cells to death receptor-induced apoptosis
    Stephan Mathas
    Max Delbruck Center for Molecular Medicine, FG Dörken, D 13125 Berlin, Germany
    J Exp Med 199:1041-52. 2004
    ..Therefore, c-FLIP is a key regulator of death receptor resistance in HRS cells...
  4. doi Aberrant expression of the Th2 cytokine IL-21 in Hodgkin lymphoma cells regulates STAT3 signaling and attracts Treg cells via regulation of MIP-3alpha
    Björn Lamprecht
    Max Delbruck Center for Molecular Medicine, Berlin, Germany
    Blood 112:3339-47. 2008
    ..Together, these data support the concept that aberrant expression of B lineage-inappropriate genes plays an important role for the biology of HL tumor cells...
  5. ncbi Classical Hodgkin lymphoma is characterized by high constitutive expression of activating transcription factor 3 (ATF3), which promotes viability of Hodgkin/Reed-Sternberg cells
    Martin Janz
    Hematology, Oncology, and Tumorimmunology, Max Delbruck Center for Molecular Medicine, Robert Rossle Str 10, 13092 Berlin, Germany
    Blood 107:2536-9. 2006
    ..Selective knock-down of ATF3 by RNA interference suppressed proliferation and strongly reduced viability of Hodgkin cells. Thus, overexpression of ATF3 is a molecular hallmark of cHL that contributes to the malignant growth of HRS cells...
  6. ncbi Intrinsic inhibition of transcription factor E2A by HLH proteins ABF-1 and Id2 mediates reprogramming of neoplastic B cells in Hodgkin lymphoma
    Stephan Mathas
    Max Delbruck Center for Molecular Medicine, 13125 Berlin, Germany
    Nat Immunol 7:207-15. 2006
    ..These data demonstrate the plasticity of mature human lymphoid cells and offer an explanation for the unique classical Hodgkin lymphoma phenotype...
  7. pmc Nuclear factor kappaB-dependent gene expression profiling of Hodgkin's disease tumor cells, pathogenetic significance, and link to constitutive signal transducer and activator of transcription 5a activity
    Michael Hinz
    Max Delbruck Center for Molecular Medicine, 13125 Berlin, Germany
    J Exp Med 196:605-17. 2002
    ..The gene profile underscores a central role of NF-kappaB in the pathogenesis of HD and potentially of other tumors with constitutive NF-kappaB activation...
  8. ncbi Reprogramming of B lymphoid cells in human lymphoma pathogenesis
    Martin Janz
    Max Delbruck Center for Molecular Medicine, Berlin, Germany
    Cell Cycle 5:1057-61. 2006
    ....
  9. ncbi The pathogenesis of classical Hodgkin's lymphoma: a model for B-cell plasticity
    Stephan Mathas
    Max Delbruck Center for Molecular Medicine, Robert Rossle Str 10, 13125 Berlin, Germany
    Hematol Oncol Clin North Am 21:787-804. 2007
    ..HRS cells might be reprogrammed into cells resembling undifferentiated progenitor cells, which might offer an explanation for the unique HL phenotype and demonstrate a high degree of plasticity of human lymphoid cells...
  10. pmc Gene deregulation and spatial genome reorganization near breakpoints prior to formation of translocations in anaplastic large cell lymphoma
    Stephan Mathas
    Max Delbruck Center for Molecular Medicine, Robert Rossle Strasse 10, 13125 Berlin, Germany
    Proc Natl Acad Sci U S A 106:5831-6. 2009
    ..Also, our data demonstrate that deregulation of breakpoint-proximal genes has a key role in ALCL...
  11. doi Derepression of an endogenous long terminal repeat activates the CSF1R proto-oncogene in human lymphoma
    Björn Lamprecht
    Max Delbruck Center for Molecular Medicine, Berlin, Germany
    Nat Med 16:571-9, 1p following 579. 2010
    ..We conclude that LTR derepression is involved in the pathogenesis of human lymphomas, a finding that might have diagnostic, prognostic and therapeutic implications...
  12. pmc Repeat-element driven activation of proto-oncogenes in human malignancies
    Björn Lamprecht
    Max Delbruck Center for Molecular Medicine, Charite Universitatsmedizin Berlin, Germany
    Cell Cycle 9:4276-81. 2010
    ..This article summarizes these results and gives an outlook on the impact of these findings on the pathogenesis and therapy of human cancer...
  13. doi The dangers of transcription
    Stephan Mathas
    Max Delbruck Center for Molecular Medicine, 13125 Berlin, Germany
    Cell 139:1047-9. 2009
    ..In this issue, Lin et al. (2009) provide evidence that binding of the transcription machinery may predispose genome regions to breakage and translocations that may lead to cancer...
  14. ncbi A rapamycin derivative (everolimus) controls proliferation through down-regulation of truncated CCAAT enhancer binding protein {beta} and NF-{kappa}B activity in Hodgkin and anaplastic large cell lymphomas
    Franziska Jundt
    Charite, Campus Virchow Klinikum, University Medicine Berlin, Augustenburger Platz 1, D 13 353 Berlin, Germany
    Blood 106:1801-7. 2005
    ..Pharmacologic inhibition of the mTOR pathway by RAD therefore interferes with essential proliferation and survival pathways in HL and ALCL cells and might serve as a novel treatment option...
  15. pmc Aberrantly expressed c-Jun and JunB are a hallmark of Hodgkin lymphoma cells, stimulate proliferation and synergize with NF-kappa B
    Stephan Mathas
    Max Delbrück Center for Molecular Medicine and Universitätsklinikum Charité, Robert Rossle Klinik, Humboldt University, Lindenberger Weg 80, D 13125 Berlin
    EMBO J 21:4104-13. 2002
    ..Together, these data suggest an important role of AP-1 in lymphoma pathogenesis...
  16. ncbi Activated Notch1 signaling promotes tumor cell proliferation and survival in Hodgkin and anaplastic large cell lymphoma
    Franziska Jundt
    Charite, Robert Rossle Klinik, Humboldt University of Berlin, Germany
    Blood 99:3398-403. 2002
    ..Thus, our data suggest that activated Notch1 signaling plays an important role in the pathobiology of Hodgkin and anaplastic large cell lymphoma and that it might be a potential new target for treatment...
  17. ncbi Loss of PU.1 expression is associated with defective immunoglobulin transcription in Hodgkin and Reed-Sternberg cells of classical Hodgkin disease
    Franziska Jundt
    Charite, Robert Rossle Klinik, Humboldt University of Berlin, Germany
    Blood 99:3060-2. 2002
    ..Our study identifies PU.1 deficiency as a recurrent defect in HRS cells that might contribute to their impairment of immunoglobulin transcription...
  18. ncbi Dendritic cell maturation stage determines susceptibility to the proteasome inhibitor bortezomib
    Marion Subklewe
    Charite, Universitaetsmedizin Berlin, Campus Virchow Klinikum, Med Klinik m S Haematologie Onkologie, Berlin, Germany
    Hum Immunol 68:147-55. 2007
    ..Our findings suggest a potential role of bortezomib in modulating immune responses in humans through inhibition of DC maturation...
  19. ncbi Jagged1-induced Notch signaling drives proliferation of multiple myeloma cells
    Franziska Jundt
    Department of Hematology and Oncology, Charite, Campus Virchow Klinikum, University Medicine Berlin, Berlin, Germany
    Blood 103:3511-5. 2004
    ..Functional data indicate that ligand-induced Notch signaling is a growth factor for MM cells and suggest that these interactions contribute to myelomagenesis in vivo...
  20. ncbi In the presence of bone marrow stromal cells human multiple myeloma cells become independent of the IL-6/gp130/STAT3 pathway
    Manik Chatterjee
    Department of Hematology, Oncology, and Tumorimmunology, Robert Rössle Cancer Center at the Max Delbrück Center for Molecular Medicine, Charite, Humboldt University Berlin, Campus Berlin Buch, Linderberger Weg 80, D 13122 Berlin, Germany
    Blood 100:3311-8. 2002
    ..Furthermore, we provide evidence that farnesyl transferase inhibitors might be useful for the development of novel therapeutic strategies for the treatment of MM...