Notch signaling as a target in multimodality cancer therapy

Curr Opin Mol Ther. 2000 Feb;2(1):55-65.

Abstract

Notch signaling is an extremely conserved and widely used mechanism controlling cell fate determination. Recent evidence shows that Notch receptors regulate cell differentiation, proliferation and apoptosis in many cells, including neoplastic cells. In the context of cancer experimental immunotherapy and multimodality therapy, the Notch signaling network is acquiring increasing importance for its possible roles in both neoplastic cells and the immune system. In this review, we discuss: (i) the roles of Notch signaling in cancer cells and the immune system; and (ii) strategies through which Notch-targeting biologicals may be used to increase the effectiveness of multimodality cancer treatment, including cancer vaccines.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.
  • Review

MeSH terms

  • Animals
  • Antibodies, Monoclonal / therapeutic use
  • Combined Modality Therapy
  • DNA, Antisense / therapeutic use
  • DNA-Binding Proteins / physiology
  • Dendritic Cells / immunology
  • Genetic Therapy
  • Hematopoietic Stem Cell Transplantation
  • Humans
  • Immunoglobulin J Recombination Signal Sequence-Binding Protein
  • Ligands
  • Membrane Proteins / antagonists & inhibitors
  • Membrane Proteins / genetics
  • Membrane Proteins / physiology*
  • Neoplasms / immunology
  • Neoplasms / physiopathology
  • Neoplasms / therapy*
  • Nuclear Proteins*
  • Receptor, Notch1
  • Receptors, Cell Surface*
  • Receptors, Notch
  • Recombinant Proteins / therapeutic use
  • Signal Transduction
  • Transcription Factors*

Substances

  • Antibodies, Monoclonal
  • DNA, Antisense
  • DNA-Binding Proteins
  • Immunoglobulin J Recombination Signal Sequence-Binding Protein
  • Ligands
  • Membrane Proteins
  • NOTCH1 protein, human
  • Nuclear Proteins
  • RBPJ protein, human
  • Receptor, Notch1
  • Receptors, Cell Surface
  • Receptors, Notch
  • Recombinant Proteins
  • Transcription Factors