[Receptor tyrosine kinases in Hodgkin lymphoma as possible therapeutic targets]

Pathologe. 2009 Sep;30(5):393-400. doi: 10.1007/s00292-009-1157-9.
[Article in German]

Abstract

Hodgkin lymphoma (HL) is the most frequent nodal lymphoma in Europe. The B-cell derived Hodgkin-Reed Sternberg (HRS) cells are nearly completely deficient for expression of B-cell markers. Epstein-Barr virus (EBV) can be detected in about 40% of HL cases. Presumably, EBV protects HRS cell precursors from apoptosis. Histologically only single HRS cells are dispersed in a broad reactive cellular background. Interactions between HRS cells and their surrounding cellular infiltrate, among them paracrine activation of several signalling pathways, is crucial in HL. HRS cells also show autocrine activation of several signalling pathways. Among these, the aberrant expression and activation of seven different receptor tyrosine kinases (RTK) is of special interest, as many different antibodies and low molecular substances which inhibit RTK activity are already in clinical use for anticancer therapy. Therefore, blocking of RTK activities in HL may be a novel therapeutic option.

Publication types

  • English Abstract
  • Review

MeSH terms

  • Antineoplastic Agents / therapeutic use*
  • Autocrine Communication / genetics
  • B-Lymphocytes / pathology
  • Benzamides
  • Biopsy
  • Cell Line, Tumor
  • DNA Mutational Analysis
  • Epstein-Barr Virus Infections / drug therapy
  • Epstein-Barr Virus Infections / genetics
  • Epstein-Barr Virus Infections / pathology
  • Hodgkin Disease / drug therapy
  • Hodgkin Disease / genetics*
  • Hodgkin Disease / pathology*
  • Humans
  • Imatinib Mesylate
  • Lymph Nodes / pathology
  • Paracrine Communication / genetics
  • Piperazines / therapeutic use*
  • Pyrimidines / therapeutic use*
  • Receptor Protein-Tyrosine Kinases / antagonists & inhibitors*
  • Receptor Protein-Tyrosine Kinases / genetics*
  • Reed-Sternberg Cells / pathology
  • Signal Transduction / genetics
  • T-Lymphocytes / pathology
  • Transcription, Genetic / genetics

Substances

  • Antineoplastic Agents
  • Benzamides
  • Piperazines
  • Pyrimidines
  • Imatinib Mesylate
  • Receptor Protein-Tyrosine Kinases