title: Expression of programmed cell death proteins in patients with chronic myeloid leukemia.
abstract: OBJECTIVE
  Chronic myelogenous leukemia (CML) is a malignant myeloproliferative disease developing out of pluripotent hematopoietic stem cells that contain the fusion Bcr-Abl gene. The mechanisms that lead to these changes at molecular level are still unknown as are the mechanisms that increase the proliferative capacity of these cells. Disorders that occur in the process of apoptosis represent one of the possible molecular mechanisms that bring about disease progress. In our study we analyzed the presence of mutated (mut) p53 gene and the amplification of Bax proteins in patients with CML.
  
  
  METHODS
  This study included 30 patients with CML (23 in chronic phase, 7 in blast transformation). Using immunohistochemistry with alkaline phosphatase / anti-alkaline phosphatase (APAAP) method we analyzed the expression of cell death proteins p53 and Bax in mononuclear bone marrow cells. Polymerase chain reaction single strand conformation polymorphism (PCR-SSCP) method was used to analyze the presence of mut p53 gene in mononuclear peripheral blood cells. Reverse transcription-polymerase chain reaction (RT-PCR) method was used to analyze the presence of Bcr-Abl in peripheral blood cells.
  
  
  RESULTS
  High expression of Bax protein was detected in all analyzed patients, but no significant differences were noticed among them. No mut p53 gene was detected in any of the analyzed samples. Bcr-Abl b3a2 protein form was detected in all patients with variant translocations.
  
  
  CONCLUSIONS
  Lack of mut p53 product in the peripheral blood and bone marrow cells in patients with CML suggests that this gene plays no important role in disease pathology. Increased level of Bax protein expression is an essential characteristic of CML cells but it is not related with the clinical stage of disease.
authors.affiliation: Institute of Pathology, Military Medical Academy, Belgrade, Serbia. milicastrnad@hotmail.com
authors.forename: M
authors.initials: M
authors.lastname: Strnad
authors.forename: G
authors.initials: G
authors.lastname: Brajuskovic
authors.forename: N
authors.initials: N
authors.lastname: Strelic
authors.forename: B
authors.initials: B
authors.lastname: Todoric-Zivanovic
authors.forename: D
authors.initials: D
authors.lastname: Stamatovic
authors.forename: Z
authors.initials: Z
authors.lastname: Tatomirovic
authors.forename: Z
authors.initials: Z
authors.lastname: Magic
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D000469:Alkaline Phosphatase / Q000378:metabolism; D017209:Apoptosis / Q000235:genetics*; D001752:Blast Crisis; D002869:Chromosome Aberrations; D020732:Cytogenetic Analysis; D005260:Female; D016044:Fusion Proteins, bcr-abl / Q000235:genetics; D006801:Humans; D007124:Immunoenzyme Techniques; D015464:Leukemia, Myelogenous, Chronic, BCR-ABL Positive / Q000235:genetics* / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D009154:Mutation / Q000235:genetics; D016133:Polymerase Chain Reaction; D018807:Polymorphism, Single-Stranded Conformational; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D016159:Tumor Suppressor Protein p53 / Q000235:genetics* / Q000378:metabolism; D055815:Young Adult; D051028:bcl-2-Associated X Protein / Q000235:genetics* / Q000378:metabolism
chemical_list: C494826:BAX protein, human; D012333:RNA, Messenger; D016159:Tumor Suppressor Protein p53; D051028:bcl-2-Associated X Protein; D016044:Fusion Proteins, bcr-abl; D000469:Alkaline Phosphatase