Coexpression of genes involved in apoptosis in central nervous system neoplasms

被引:15
作者
Bruggers, CS
Fults, D
Perkins, SL
Coffin, CM
Carroll, WL
机构
[1] Univ Utah, Primary Childrens Med Ctr, Sch Med,Huntsman Canc Inst,Ctr Children, Dept Pediat,Div Hematol Oncol, Salt Lake City, UT 84113 USA
[2] Univ Utah, Primary Childrens Med Ctr, Sch Med,Huntsman Canc Inst,Ctr Children, Dept Pathol, Salt Lake City, UT 84113 USA
[3] Univ Utah, Primary Childrens Med Ctr, Sch Med,Huntsman Canc Inst,Ctr Children, Dept Neurosurg, Salt Lake City, UT 84113 USA
关键词
brain tumors; apoptosis; BCL2; BAX; BCLX; p53;
D O I
10.1097/00043426-199901000-00005
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Purpose: Apoptosis plays a crucial role in normal development and mediates tumor response to chemotherapy. This study investigated the pattern of apoptotic gene expression in brain tumor tissue specimens and cell lines. Materials and Methods: BCL2, BCLXL, BCLXS, and BAX transcripts were amplified using reverse transcriptase polymerase chain reaction in 7 high-grade gliomas (HGGs), 7 ependymomas, and 6 cell lines (2 glioblastomas, 3 medulloblastomas, and 1 supratentorial-primitive neuroectodermal tumor [PNET]). Immunohistochemical staining for BCL2, BCLX, BAX, and p53 was performed in 7 pediatric low-grade gliomas (LGGs) and 7 pediatric HGGs. Results: Six of seven gliomas, all ependymomas, and all glioblastoma and medulloblastoma cell lines expressed BCLXL and BAX. BCL2 expression was only detected in the supratentorial PNET Line PFSK. BCLXS was absent in all tumors. By immunohistochemistry, no glial tumors stained positively for BCL2. Similar BAX and BCLX protein expression was observed in LGG and HGG. Three of five glioblastomas showed significant p53 expression. Conclusions: Coexpression of proapoptotic and antiapoptotic genes in human brain tumors supports the hypothesis that the relative expression of competing genes determines apoptotic threshold.
引用
收藏
页码:19 / 25
页数:7
相关论文
共 34 条
[21]   EXPRESSION OF BCL-2 IN REACTIVE AND NEOPLASTIC ASTROCYTES - LACK OF CORRELATION WITH PRESENCE OR DEGREE OF MALIGNANCY [J].
KRISHNA, M ;
SMITH, TW ;
RECHT, LD .
JOURNAL OF NEUROSURGERY, 1995, 83 (06) :1017-1022
[22]   The proto-oncogene Bcl-2 and its role in regulating apoptosis [J].
Kroemer, G .
NATURE MEDICINE, 1997, 3 (06) :614-620
[23]   p53, the cellular gatekeeper for growth and division [J].
Levine, AJ .
CELL, 1997, 88 (03) :323-331
[24]   BCL-2-IMMUNOGLOBULIN TRANSGENIC MICE DEMONSTRATE EXTENDED B-CELL SURVIVAL AND FOLLICULAR LYMPHOPROLIFERATION [J].
MCDONNELL, TJ ;
DEANE, N ;
PLATT, FM ;
NUNEZ, G ;
JAEGER, U ;
MCKEARN, JP ;
KORSMEYER, SJ .
CELL, 1989, 57 (01) :79-88
[25]   EVOLUTION OF THE FUNCTIONAL HUMAN BETA-ACTIN GENE AND ITS MULTI-PSEUDOGENE FAMILY - CONSERVATION OF NONCODING REGIONS AND CHROMOSOMAL DISPERSION OF PSEUDOGENES [J].
NG, SY ;
GUNNING, P ;
EDDY, R ;
PONTE, P ;
LEAVITT, J ;
SHOWS, T ;
KEDES, L .
MOLECULAR AND CELLULAR BIOLOGY, 1985, 5 (10) :2720-2732
[26]   BCL-2 HETERODIMERIZES IN-VIVO WITH A CONSERVED HOMOLOG, BAX, THAT ACCELERATES PROGRAMMED CELL-DEATH [J].
OLTVAI, ZN ;
MILLIMAN, CL ;
KORSMEYER, SJ .
CELL, 1993, 74 (04) :609-619
[27]  
Pollack IF, 1997, CANCER RES, V57, P304
[28]   PROGRAMMED CELL-DEATH AND THE CONTROL OF CELL-SURVIVAL - LESSONS FROM THE NERVOUS-SYSTEM [J].
RAFF, MC ;
BARRES, BA ;
BURNE, JF ;
COLES, HS ;
ISHIZAKI, Y ;
JACOBSON, MD .
SCIENCE, 1993, 262 (5134) :695-700
[29]  
Reed JC, 1997, SEMIN HEMATOL, V34, P9
[30]   BCL2-MEDIATED TUMORIGENICITY OF A HUMAN T-LYMPHOID CELL-LINE - SYNERGY WITH MYC AND INHIBITION BY BCL2 ANTISENSE [J].
REED, JC ;
CUDDY, M ;
HALDAR, S ;
CROCE, C ;
NOWELL, P ;
MAKOVER, D ;
BRADLEY, K .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1990, 87 (10) :3660-3664