title: The clinical significance of soluble CD86 levels in patients with acute myeloid leukemia and myelodysplastic syndrome.
abstract: BACKGROUND
  Levels of the soluble form of CD86 (sCD86) are elevated in a proportion of patients with leukemia. Although it is a potential modulator of antitumor responses, the significance of sCD86 in patients with hematologic malignancies is unknown.
  
  
  METHODS
  The authors evaluated sCD86 levels by enzyme-linked immunosorbent assay in patients with acute myeloid leukemia (AML) (n = 57 patients) and patients with myelodysplastic syndrome (MDS) (n = 40 patients) and analyzed the relation between sCD86 levels and various clinical parameters.
  
  
  RESULTS
  Levels of sCD86 were elevated (> 2.32 ng/mL) relative to normal donors (0.22-2.32 ng/mL; n = 51 patients) in 25% of patients with AML and in 27% of patients with MDS. Patients with AML who had elevated sCD86 levels had significantly lower complete remission (CR) rates compared with patients with AML who had normal sCD86 levels. In multivariate analysis using sCD86 as a continuous variable and including the interaction of age and sCD86 as a variable, sCD86 was a significant prognostic factor (P = 0.014) independent of cytogenetics. Further analysis demonstrated that, in patients with AML age 60 years and younger, but not in patients older than 60 years, elevated sCD86 levels were associated with significantly shorter survival (P = 0.04). There was no correlation between sCD86 levels and CR rates or survival in patients with MDS.
  
  
  CONCLUSIONS
  The presence in patients with AML of elevated levels of circulating sCD86 were associated with lower CR rates and poor survival. The prognostic significance of sCD86 was independent of cytogenetics but was modulated by age, in that it was independently significant only in younger patients. The results suggest that sCD86 may play a role in modulating immune responses associated with the progression of AML.
authors.affiliation: Haematology Research Group, Christchurch Hospital, Christchurch, New Zealand. barry.hock@chmeds.ac.nz
authors.forename: Barry D
authors.initials: BD
authors.lastname: Hock
authors.forename: Judith L
authors.initials: JL
authors.lastname: McKenzie
authors.forename: William Nigel
authors.initials: WN
authors.lastname: Patton
authors.forename: Lisa F
authors.initials: LF
authors.lastname: Haring
authors.forename: Ying
authors.initials: Y
authors.lastname: Yang
authors.forename: Yu
authors.initials: Y
authors.lastname: Shen
authors.forename: Elihu H
authors.initials: EH
authors.lastname: Estey
authors.forename: Maher
authors.initials: M
authors.lastname: Albitar
mesh_terms: D000293:Adolescent; D000328:Adult; D015703:Antigens, CD / Q000097:blood*; D051940:B7-2 Antigen; D005260:Female; D006801:Humans; D015470:Leukemia, Myeloid, Acute / Q000097:blood* / Q000401:mortality; D008297:Male; D008562:Membrane Glycoproteins / Q000097:blood*; D008875:Middle Aged; D009190:Myelodysplastic Syndromes / Q000097:blood* / Q000401:mortality; D011379:Prognosis; D015996:Survival Rate
chemical_list: D015703:Antigens, CD; D051940:B7-2 Antigen; C497964:CD86 protein, human; D008562:Membrane Glycoproteins