A humanised anti-IGF-1R monoclonal antibody (AVE1642) enhances Bortezomib-induced apoptosis in myeloma cells lacking CD45

Br J Cancer. 2009 Jan 27;100(2):366-9. doi: 10.1038/sj.bjc.6604839.

Abstract

The humanised form of an antagonistic anti-IGF-1R mAb (AVE1642) selectively inhibits the growth of CD45(neg) myeloma cells. AVE1642 strongly increased bortezomib-induced apoptosis, correlated with an increase of Noxa expression. These results support the therapeutic use of anti-IGF-1R/bortezomib in CD45(neg) Myeloma patients, particularly those with the most aggressive form, t(4,14).

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Antibodies, Monoclonal / pharmacology*
  • Antineoplastic Agents / pharmacology*
  • Apoptosis / drug effects*
  • Apoptosis / immunology
  • Boronic Acids / pharmacology*
  • Bortezomib
  • Caspase 3 / metabolism
  • Cell Proliferation / drug effects
  • Enzyme Activation / drug effects
  • Humans
  • Leukocyte Common Antigens / metabolism*
  • Multiple Myeloma / drug therapy
  • Multiple Myeloma / immunology
  • Multiple Myeloma / pathology*
  • Proto-Oncogene Proteins c-bcl-2 / metabolism
  • Pyrazines / pharmacology*
  • Receptor, IGF Type 1 / immunology*
  • Tumor Cells, Cultured

Substances

  • Antibodies, Monoclonal
  • Antineoplastic Agents
  • Boronic Acids
  • PMAIP1 protein, human
  • Proto-Oncogene Proteins c-bcl-2
  • Pyrazines
  • Bortezomib
  • Receptor, IGF Type 1
  • Leukocyte Common Antigens
  • Caspase 3