Bcl-2 Inhibits T-Cell-mediated Cytolysis of a Leukemia Cell Line

Academic Article


  • The bcl-2 gene becomes deregulated in its expression in a wide variety of human cancers and has been shown to block both spontaneous and drug-induced cell death, thus conferring a selective survival advantage on malignant cells. The biochemical mechanism by which bcl-2 promotes cell survival remains enigmatic but appears to involve a downstream event in an evolu-tionarily conserved cell death pathway. Here we report that gene transfer-mediated increases in Bcl-2 protein levels in the human leukemia line Jurkat render these cells more resistant to induction of DNA fragmentation and cytolysis by a cloned T-celL The killing mechanism used by these particular T-cells was consistent with apoptosis, as opposed to necrosis, in that DNA degradation occurred as a prelysis event The findings raise the possibility that dysregulation of bcl-2 gene expression could play a role in the avoidance of immune surveillance mechanisms by cancer cells. © 1994, American Association for Cancer Research. All rights reserved.
  • Published In

  • Cancer Research  Journal
  • Author List

  • Torigoe T; Millan JA; Takayama S; Taichman R; Miyashita T; Reed JC
  • Start Page

  • 4851
  • End Page

  • 4854
  • Volume

  • 54
  • Issue

  • 18