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Differential expression of cell proliferation regulatory proteins in B‐ and T‐lineage acute lymphoblastic leukaemias
Author(s) -
WoŁowiec Dariusz,
Mekki Yahia,
Ffrench Patrick,
Manel AnneMarie,
Bertrand Yves,
Rimokh Ruth,
Philippe Noel,
Bryon PaulAndré,
Ffrench Martine
Publication year - 1996
Publication title -
british journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.907
H-Index - 186
eISSN - 1365-2141
pISSN - 0007-1048
DOI - 10.1046/j.1365-2141.1996.d01-1930.x
Subject(s) - cyclin dependent kinase 6 , biology , proliferating cell nuclear antigen , cyclin , cell growth , cyclin dependent kinase 1 , lineage (genetic) , cancer research , lineage markers , cell cycle , cyclin b , microbiology and biotechnology , bone marrow , cyclin d , apoptosis , immunology , genetics , progenitor cell , stem cell , gene
In order to better understand the molecular background of differences between the clinical picture of T‐ and B‐lineage ALLs, we studied the expression of several proteins involved in the regulation of cell proliferation in bone marrow blast cells from 30 cases of previously untreated acute lymphoblastic leukaemia (ALL); 14 cases were T‐ and 16 B‐cell lineage ALLs. We studied several cyclin‐dependent kinases (cdk1, cdk2, cdk4, cdk6) and cyclins (cyclin A, cyclin B1, cyclin D3 and cyclin E). We also studied proliferating cell nuclear antigen (PCNA) and Bcl‐2 expression, the latter protein known to be involved in the prolonged survival of B‐lineage ALL blasts. Proteins obtained from cell lysates were resolved on polyacrylamide gel followed by immunodetection and densitometry of specific bands. Expression of cdk1 and PCNA, markers of proliferative activity, was significantly higher in T‐ than in B‐lineage ALL. Cdk6, which was highly correlated to PCNA, was also higher in T‐cell ALL. In contrast, B‐lineage ALL displayed a higher expression of anti‐apoptotic protein Bcl‐2. We hypothesize that those particularities may reflect differential roles of cell multiplication and apoptosis in the neoplastic proliferation of B‐ and T‐lineage ALL.