Amplification and expression of a decoy receptor for fas ligand (DcR3) in virus (EBV or HTLV-I) associated lymphomas

Cancer Lett. 2000 Nov 10;160(1):89-97. doi: 10.1016/s0304-3835(00)00567-x.


The recently identified decoy receptor 3 (DcR3) binds to FasL and inhibits FasL-induced apoptosis, and is considered to play a role in the immune escape system of neoplastic cells. To examine the involvement of DcR3 in the immune evasions of virus-associated lymphoma, we analyzed the amplification and expression of DcR3, using dot blot and in situ hybridization (ISH), in 45 cases, which included 17 cases with Epstein-Barr virus (EBV)-associated lymphoma (seven pyothorax-associated B-cell lymphomas (PAL); ten natural killer lymphoma (NKL)), seven cases with adult T-cell leukemia lymphoma (ATLL), 13 Hodgkin's disease (eight EBV-associated cases; five non-EBV-associated cases), and eight control cases (three reactive lymphadenopathy; five non-EBV-associated-B-cell lymphoma). EBV-associated PAL and NKL exhibited DcR3 amplification and expression in lymphoma cells. ATLL also showed DcR3 expression and amplification. The cases with DcR3 amplification showed DcR3 expression; however, the expression was confined in the neoplastic cells, but not in the reactive cells. In Hodgkin's disease (HD), DcR3 was expressed only in Hodgkin and Reed-Sternberg giant (H-RS) cells. However, DcR3 was not expressed or amplified in reactive lymphadenopathy. Non-EBV-associated B-cell lymphoma also rarely expressed DcR3, and showed no amplification except in two cases, in which rare expression was present. Our results suggest that EBV and HTLV-I probably use DcR3 to escape from the immune system during lymphomagenesis, or virus-infected lymphoma cells with DcR3 expression might be selected in the multistep tumorigenesis.

MeSH terms

  • Adolescent
  • Adult
  • Aged
  • Aged, 80 and over
  • Burkitt Lymphoma / genetics*
  • Burkitt Lymphoma / pathology
  • Burkitt Lymphoma / virology
  • Child
  • Fas Ligand Protein
  • Female
  • Gene Amplification
  • Gene Expression Regulation, Neoplastic
  • Genotype
  • Herpesvirus 4, Human / genetics
  • Hodgkin Disease / genetics
  • Hodgkin Disease / pathology
  • Humans
  • In Situ Hybridization
  • Leukemia-Lymphoma, Adult T-Cell / genetics*
  • Leukemia-Lymphoma, Adult T-Cell / pathology
  • Leukemia-Lymphoma, Adult T-Cell / virology
  • Male
  • Membrane Glycoproteins / metabolism
  • Middle Aged
  • Nucleic Acid Hybridization / methods
  • Phenotype
  • RNA, Neoplasm / genetics
  • RNA, Neoplasm / metabolism
  • RNA, Viral / genetics
  • RNA, Viral / metabolism
  • Receptors, Cell Surface / genetics*
  • Receptors, Cell Surface / metabolism
  • Receptors, Tumor Necrosis Factor
  • Receptors, Tumor Necrosis Factor, Member 6b


  • FASLG protein, human
  • Fas Ligand Protein
  • Membrane Glycoproteins
  • RNA, Neoplasm
  • RNA, Viral
  • Receptors, Cell Surface
  • Receptors, Tumor Necrosis Factor
  • Receptors, Tumor Necrosis Factor, Member 6b
  • TNFRSF6B protein, human