Expression of Bcl-2 by human bone marrow mast cells and its overexpression in mast cell leukemia
✍ Scribed by Cerver�, Carlos; Escribano, Luis; San Miguel, Jes�s F.; D�az-Agust�n, Beatriz; Bravo, Pilar; Villarrubia, Jes�s; Garc�a-Sanz, Ram�n; Velasco, Jos� L.; Herrera, Pilar; Vargas, Mario; Gonz�lez, Marcos; Navarro, Jos� L.; Orfao, Alberto
- Publisher
- John Wiley and Sons
- Year
- 1999
- Tongue
- English
- Weight
- 51 KB
- Volume
- 60
- Category
- Article
- ISSN
- 0361-8609
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✦ Synopsis
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.