Death Receptor Expression on Blasts in AML Is Associated with Unfavorable Prognosis

Anticancer Res. 2015 Jul;35(7):4043-52.

Abstract

Background: Tumor necrosis factor (TNF) receptor family members play a key role in the regulation of biological functions such as differentiation, proliferation and apoptosis of various cell types.

Materials and methods: We studied co-expression profiles of death receptors from the TNF family [TNF-related apoptosis-inducing ligand receptor (TRAILR) 1 to 3, TNF receptor 1 (TNFR1) and FAS receptor (FAS)] on peripheral blood blasts from 46 patients with acute myeloid leukemia (AML) at first diagnosis by flow cytometry and correlated the obtained specific fluorescence indices (SFI) with morphological, cytogenetic and clinical parameters.

Results: We found that the expression of TRAILR2 and R3 was significantly increased in unfavorable risk groups, according to the National Comprehensive Cancer Network. Additionally, cut-off analyses for TRAILR2 and TNFR1 showed significantly shorter overall survival, earlier disease onset, higher proportions of cases with unfavorable prognosis and higher probability of relapse when SFIs were above the established cut-off.

Conclusion: We demonstrate that high co-expression of death receptors on blasts is an independent predictor of poor prognosis in AML.

Keywords: Acute myeloid leukemia; FAS; TNFR1; TRAILR; death receptors.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adolescent
  • Adult
  • Aged
  • Aged, 80 and over
  • Female
  • Humans
  • Leukemia, Myeloid, Acute / diagnosis
  • Leukemia, Myeloid, Acute / metabolism*
  • Leukemia, Myeloid, Acute / pathology
  • Male
  • Middle Aged
  • Prognosis
  • Receptors, Death Domain / metabolism*
  • Receptors, Tumor Necrosis Factor, Type I / metabolism
  • Tumor Necrosis Factor Decoy Receptors / metabolism
  • Young Adult
  • fas Receptor / metabolism

Substances

  • Receptors, Death Domain
  • Receptors, Tumor Necrosis Factor, Type I
  • Tumor Necrosis Factor Decoy Receptors
  • fas Receptor