MORPHOLOGICAL, IMMUNOCYTOCHEMICAL AND GROWTH-CHARACTERISTICS OF 3 HUMAN GLIOBLASTOMAS ESTABLISHED INVITRO

被引:47
作者
BILZER, T
STAVROU, D
DAHME, E
KEIDITSCH, E
BURRIG, KF
ANZIL, AP
WECHSLER, W
机构
[1] UNIV HAMBURG,DEPT NEUROPATHOL,W-2000 HAMBURG 13,GERMANY
[2] UNIV MUNICH,INST VET PATHOL,W-8000 MUNICH 2,GERMANY
[3] TECH UNIV MUNICH,CLINICUM BOGENHAUSEN,INST PATHOL,W-8000 MUNICH 2,GERMANY
[4] UNIV DUSSELDORF,INST PATHOL,W-4000 DUSSELDORF 1,GERMANY
[5] SUNY HLTH SCI CTR,DEPT PATHOL,BROOKLYN,NY
关键词
GLIOMA ANTIGENS; EPIDERMAL GROWTH FACTOR RECEPTOR; NERVE GROWTH FACTOR RECEPTOR; TRANSFERRIN RECEPTOR; CHROMOSOMES;
D O I
10.1007/BF01600156
中图分类号
R602 [外科病理学、解剖学]; R32 [人体形态学];
学科分类号
100101 ;
摘要
The human glioblastoma-derived cell lines 86HG-39, 87HG-28 and 87HG-31, used for the production of monoclonal antibodies (mAbs) against glioma-associated antigens (GAA), were characterized in terms of morphology, growth behaviour, chromosomes and antigen expression. In the primary tumours, differential expression of glial fibrillary acidic protein, S100 protein, Leu-7 and GAA as defined by mAbs MUC 2-39, MUC 2-63 and MUC 8-22 was demonstrated. Receptors for epidermal growth factor (EGFr) and nerve growth factor (NGFr) were found in many cells in short-term cultures, but the transferrin receptor (Tr) was found in only a few cells of 87HG-28. In permanent cell lines, differentiation antigens and EGFr decreased and Tr increased markedly. NGFr and GAA remained stable. Transplantation tumours of 86HG-39 were partly positive for Tr and GAA. Chromosomal analysis revealed that the 86HG-39 and 87HG-28 cell lines had a hypodiploid or diploid stem line with lines in the hypotetraploid to tetraploid region for 50 in vitro passages. The 87HG-31 cell line had chromosomal patterns in the hypotriploid to triploid region. A gain of chromosomes was seen in the groups C7, C8, C10, D14, F19, F20, G21, G22. The variability of antigens in these tumours and especially during long-term cultivation probably reveals an ability to influence the growth of malignant glioma cells via the respective effector molecules.
引用
收藏
页码:281 / 293
页数:13
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