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Differences in BCL‐X L expression and STAT5 phosphorylation in chronic myeloid leukaemia patients
Author(s) -
GutiérrezCastellanos Sergio,
Cruz Miguel,
Rabelo Laura,
Godínez Rocio,
ReyesMaldonado Elba,
RiebelingNavarro Carlos
Publication year - 2004
Publication title -
european journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.904
H-Index - 84
eISSN - 1600-0609
pISSN - 0902-4441
DOI - 10.1046/j.0902-4441.2003.00201.x
Subject(s) - stat5 , chronic myeloid leukaemia , phosphorylation , cancer research , myeloid , medicine , expression (computer science) , oncology , biology , genetics , computer science , programming language
Chronic myelogenous leukaemia (CML) cells show expression of BCL‐X L , an anti‐apoptotic oncogene. This expression is induced by BCR‐ABL protein kinase through activation of the signal transducer and activator of transcription‐5 protein (STAT5). To date, however, the contribution of BCL‐X L and STAT5 to the transforming phenotype in CML is still unclear. This study was aimed at defining the status of activated STAT5 and BCL‐X L expression and their relation to BCR‐ABL rearrangement in CML cells derived from patients at different clinical stages. Twenty‐seven consecutive patients with CML were enrolled in the study. Peripheral blood mononuclear cells were lysed and subjected to immunoprecipitation and Western blotting to analyse phosphorylated STAT5. The p210 BCR‐ABL rearrangements were determined by reverse transcriptase‐polymerase chain reaction (RT‐PCR) and BCL‐X L expression by semi‐quantitative RT‐PCR. We found that increased transcription of BCL‐X L gene was associated with phosphorylated STAT5 in the majority of blast crisis patients and in a few accelerated and chronic phase patients. Moreover, BCL‐X L expression levels were found to be decreased in chronic phase, contrary to a marked increase in blast crisis. We found no difference in expression of BCL‐X L and phosphorylated STAT5 when related with b3a2 and b2a2 BCR‐ABL rearrangements. These results suggest that STAT5 activity and BCL‐X L overexpression may reflect a stage of differentiation among CML phases, and this could contribute to BCR‐ABL‐dependent transformation.