title: Soluble form of TRAIL, Fas and FasL in the serum of patients with B-CLL.
abstract: OBJECTIVE
  Although many studies demonstrated expression of TNF family members in the course of B-CLL, there is a little known about relationships between soluble forms of these proteins. Furthermore, there is no study reported on effects of used therapy on this relation. The present study was designed to asses the relationships between the serum concentrations of sFas, sFasL and sTRAIL in patients with B-CLL regarding their correlation with clinical stage and used therapy.
  
  
  METHODS
  We studied 40 patients with B-cell chronic lymphocytic leukemia (B-CLL) at diagnosis, before treatment and four weeks after therapy. To measure sFas, sFasL and sTRAIL levels in serum commercially available ELISA kits were used.
  
  
  RESULTS
  We found increased concentrations of sFas in sera of all patients with B-CLL before treatment in comparison to the control group. There were no significant differences in concentrations of sFasL and sTRAIL between patients and control group. Increased sFasL concentrations after FC and CC therapy as well as decreased concentrations after 2CdA therapy in comparison to values before treatment were found. The concentrations of sTRAIL after FC and CC therapy were higher than those in patients before treatment.
  
  
  CONCLUSIONS
  Results obtained suggest that relationship between sFas, sFasL and sTRAIL in sera of patients with B-CLL before treatment may facilitate the growth B leukemic cells. Changes in these relations after therapy with FC and CC can make a contribution to inhibit B cells growth on the apoptosis way in this patient group.
authors.affiliation: Department of Immunology, Medical University of Bialystok, Poland. ewaj@amb.edu.pl
authors.forename: E
authors.initials: E
authors.lastname: Jabłońska
authors.forename: B
authors.initials: B
authors.lastname: Kiersnowska-Rogowska
authors.forename: F
authors.initials: F
authors.lastname: Rogowski
authors.forename: A
authors.initials: A
authors.lastname: Parfieńczyk
authors.forename: W
authors.initials: W
authors.lastname: Puzewska
authors.forename: M
authors.initials: M
authors.lastname: Bukin
mesh_terms: D000971:Antineoplastic Combined Chemotherapy Protocols / Q000627:therapeutic use; D017209:Apoptosis; D051017:Apoptosis Regulatory Proteins / Q000097:blood*; D016022:Case-Control Studies; D003520:Cyclophosphamide / Q000008:administration & dosage; D053222:Fas Ligand Protein; D005260:Female; D006801:Humans; D015451:Leukemia, Lymphocytic, Chronic, B-Cell / Q000097:blood* / Q000188:drug therapy / Q000473:pathology; D008297:Male; D008562:Membrane Glycoproteins / Q000097:blood*; D008875:Middle Aged; D008942:Mitoxantrone / Q000008:administration & dosage; D012995:Solubility; D053221:TNF-Related Apoptosis-Inducing Ligand; D014409:Tumor Necrosis Factor-alpha; D048069:Tumor Necrosis Factors / Q000097:blood*; D014740:Vidarabine / Q000008:administration & dosage / Q000031:analogs & derivatives; D019014:fas Receptor / Q000097:blood*
chemical_list: D051017:Apoptosis Regulatory Proteins; C505661:FASLG protein, human; D053222:Fas Ligand Protein; D008562:Membrane Glycoproteins; D053221:TNF-Related Apoptosis-Inducing Ligand; C505653:TNFSF10 protein, human; D014409:Tumor Necrosis Factor-alpha; D048069:Tumor Necrosis Factors; D019014:fas Receptor; D003520:Cyclophosphamide; D008942:Mitoxantrone; D014740:Vidarabine; C024352:fludarabine