EXPRESSION OF THE PROLIFERATING CELL NUCLEAR ANTIGEN IN BONE-MARROW CELLS FROM PATIENTS WITH MYELODYSPLASTIC SYNDROMES AND APLASTIC-ANEMIA

被引:31
|
作者
KITAGAWA, M
KAMIYAMA, R
KASUGA, T
机构
[1] Department of Pathology, Faculty of Medicine, Tokyo Medical and Dental University, Tokyo
关键词
MYELODYSPLASTIC SYNDROME; APLASTIC ANEMIA; CELL KINETICS; IMMUNOHISTOCHEMISTRY;
D O I
10.1016/0046-8177(93)90082-R
中图分类号
R36 [病理学];
学科分类号
100104 ;
摘要
To determine the proliferative activity of the hematopoietic cells under nonneoplastic and/or neoplastic conditions, the expression of a cell cycle-related antigen, the proliferating cell nuclear antigen (PCNA), was examined in the bone marrow trephines of 79 individuals, 12 of whom had no hematologic disorder, 32 of whom had a diagnosis of myelodysplastic syndromes (MDSs), 20 of whom suffered from aplastic anemia, and 15 of whom had a diagnosis of acute myeloid leukemia. Most of the patients with MDS had more than 15% PCNA-positive cells (23.5% ± 1.5%) while patients with no hematologic disorder showed fewer than 15% PCNA-positive cells (11.7% ± 0.7%). The overall ratio of the PCNA-positive cell fraction in the bone marrow was considered of prognostic value for predicting transition into overt leukemia from MDS. Aplastic anemia cases usually exhibited hypocellular bone marrow and an infrequent labeling with the anti-PCNA antibody (3.5% ± 0.5%). However, a few aplastic anemia cases showed hypercellular bone marrow and a significantly high PCNA-positive cell ratio (32.0% ± 4.4%). In the bone marrow of acute myeloid leukemia patients more than 20% of total nucleated cells were positive for PCNA (30.0% ± 2.2%). The results suggest that the expression of PCNA is associated with the regulation of bone marrow cell proliferation and the bone marrow cellularity, and that these findings would serve as an early indicator of evolution of overt leukemia in MDS and also would be useful in distinguishing MDS cases from aplastic anemia cases when the bone marrow is hypocellular or normocellular. © 1993.
引用
收藏
页码:359 / 363
页数:5
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