BIOLOGICAL CHARACTERISTICS OF CHRONIC EOSINOPHILIC LEUKEMIA-CELLS WITH A T(2-5)(P23-Q35) TRANSLOCATION

被引:9
作者
SATO, H
SAITO, H
IKEBUCHI, K
DANBARA, M
YAGISAWA, M
YUO, A
机构
[1] Fourth Department of Internal Medicine, Teikyo University School of Medicine, Kawasaki
[2] Clinical Research Center for Rheumato-Allergology, National Sagamihara Hospital, Sagamihara
[3] Institute of Medical Science, University of Tokyo
[4] Department of Internal Medicine, Kitasato University Hospital, Sagamihara
[5] Clinical Research Institute. International Medical Center of Japan, Tokyo
关键词
CELL PHYSIOLOGY; CLONOGENIC ASSAY; CYTOGENETICS; EOSINOPHILOPOIETIC GROWTH FACTORS; HYPEREOSINOPHILIC SYNDROME;
D O I
10.3109/10428199509112211
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
We studied the biological features of eosinophils in a patient with chronic eosinophilic leukemia and a unique t(2;5)(p23;q35) translocation. Microscopic and cytochemical studies revealed no particular abnormalities, although more than 90% of the peripheral eosinophils had a density lighter than 1.080 g/ml. Clonogenic assay disclosed that myeloid progenitor cells possessed the translocation, although in vitro eosinophilopoiesis seemed normal, and there were also hematopoietic cells with a normal karyotype. In a surface marker study, EG1 was positive on 34.0% of the eosinophils, while EG2 positivity was only 0.5%. Eosinophilopoietic growth factors and adhesion molecules were virtually absent with the exception of GM-CSF and CD11b. Functional studies showed that chemotaxis for C5a was normal, although that for IL-2 or FMLP was attenuated. In addition, leukotriene C-4 production was decreased while O-2-production was intact. These findings indicated that our patient's eosinophils were not in an activated state despite their extreme hypodensity, and suggested that the leukemic eosinophils had slight defects of cellular function. These characteristics may have saved the patient from the multiple organ damage which occurs in typical hypereosinophilic syndrome.
引用
收藏
页码:499 / 505
页数:7
相关论文
共 35 条
[11]  
Kueck B.D., Smith R.E., Parkin J., Peterson L.C., Hanson C.A., Eosinophilic Leukemia: A Myeloproliferative Disorder Distinct from the Hypereosinophilic Syndrome, Hematologic Pathol., 5, pp. 195-205, (1991)
[12]  
Yoo T.J., Orman S.V., Patil S.R., Needleman C., Dorminey S., Rajtora D., Graves N., Ackerman L., Taylor W.W., Evolution to Eosinophilie Leukemia with a t(5:11) Translocation in a Patient with Hypereosinophilie Syndrome, Cancer Genet Cytogenet, 11, pp. 389-394, (1984)
[13]  
Goh K.O., Ho F.S.C., Tso S.C., Ma J., Is Hypereosinophilie Syndrome a Malignant Disease?, Cancer, 55, pp. 2395-2399, (1985)
[14]  
Cassi E., De Paoli A., Fava S., Luoni M., Tosi A., Turri C., Grimi E., Idiopathic hypereosinophilic syndrome and “eosinophilic leukemia”, Haematologica, 77, pp. 430-432, (1992)
[15]  
Bitran J.D., Rowley J.D., Plapp F., Golomb H.M., Ultmann J.E., Chromosomal Aneuploidy in a Patient with Hypereosinophilic Syndrome. Evidence for a Malignant Disease, Am. J. Med., 63, pp. 1010-1014, (1977)
[16]  
De Silva M.A.P., Heerema N., Schwenk G.R.J., Hoffman R., Evidence for the Clonal Nature of Hypereosinophilic Syndrome, Cancer Genet Cytogenet., 32, pp. 109-115, (1988)
[17]  
Wolz D.E., Granato J.E., Giles H.R., Marks S.M., Grill H.P., A unique chromosomal abnormality in idiopathic hypercosinophilic syndrome presenting with cardiac involvement, Am. Heart J., 126, pp. 246-248, (1993)
[18]  
Sato H., Danbara M., Tamura M., Morita M., Eosinophilic Leukaemia with a t(2
[19]  
5)(p23:q35) translocation, Br. J. Haematol., 87, pp. 404-406, (1994)
[20]  
Brown N.J., Stein R.S., Idiopathic Hypereosinophilic Syndrome Progressing to Acute Myelomonocytic Leukemia With Chloroma, Southern Med. J., 82, pp. 1303-1305, (1989)