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Expression of Bcl-2 by human bone marrow mast cells and its overexpression in mast cell leukemia

1999; Wiley; Volume: 60; Issue: 3 Linguagem: Inglês

10.1002/(sici)1096-8652(199903)60

1096-8652

Carlos Cerver�, L. Escribano, Jesús F. San Miguel, Beatriz D�az-Agust�n, Pilar Bravo, Jesús Villarrubia, Ram�n Garc�a-Sanz, Jos� L. Velasco, Pilar Herrera, Mario Bautista-Vargas, Marcos Gonz�lez, Jos� L. Navarro, Alberto Orfao,

Click Chemistry and Applications

Bcl-2 protein plays a major role in the prevention of programmed cell death of differentiating cells. In the present study, the expression of cytoplasmic bcl-2 by human Bone Marrow Mast Cells (BMMC) from both normal and pathological bone marrow samples was examined. A total of 35 subjects corresponding to 9 healthy volunteers, 8 cases of adult indolent systemic mast cell disease (SMCD), 4 cases of pediatric mastocytosis (PM), 11 cases of hematological malignancies (HM), 2 cases of reactive bone marrow, and 1 case of mast cell leukemia (MCL) were analyzed. The expression of bcl-2 was studied using quantitative three-color flow cytometry. We also studied the molecular configuration of the bcl-2 gene and other relatives by Southern blot and polymerase chain reaction (PCR) in the MCL case. Bcl-2 expression was detected in BMMC from all samples analyzed. No significant differences on the expression of bcl-2 were detected between BMMC from healthy subjects and patients with SMCD, PM, HM, and reactive bone marrow. By contrast, bcl-2 protein was overexpressed in BMMC from MCL patient without gene rearrangement. Our results show that bcl-2 protein was constitutively expressed by BMMC. BMMC from MCL display overexpression of bcl-2, which could not be related to molecular rearrangements involving the bcl-2 gene. The expression of this protein by mature MC may play a role in the prevention of MC apoptosis and thus help to explain the long survival of these cells. The overexpression of bcl-2 by BMMC in MCL may help to explain their resistance to chemotherapy-induced apoptosis. Am. J. Hematol. 60:191–195, 1999. © 1999 Wiley-Liss, Inc.