Bcl-2-related genes in lymphoid neoplasia

被引:28
作者
Wei, MC
机构
[1] Harvard Univ, Sch Med, Childrens Hosp, Dept Med, Boston, MA 02125 USA
[2] Boston Univ, Sch Med, Dept Pediat, Boston Med Ctr, Boston, MA 02118 USA
关键词
Bcl-2; apoptosis; leukemia; lymphoma;
D O I
10.1532/IJH97.04110
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
The proto-oncogene BCL-2 was discovered with the cloning of the t(14;18) chromosomal translocation responsible for human follicular lymphoma. Since then other members of the Bcl-2 family of cell death regulators have been identified and their roles in cell death, normal lymphoid development, and lymphoid neoplasia have been characterized. Bcl-2 family members are important in tumor initiation, progression, and response to chemotherapy, and altered expression levels of various members serve as prognostic markers in many lymphoid malignancies. There are promising cancer therapeutics now targeted at members of the Bcl-2 family. (C) 2004 The Japanese Society of Hematology.
引用
收藏
页码:205 / 209
页数:5
相关论文
共 57 条
[1]   CLONING THE CHROMOSOMAL BREAKPOINT OF T(14-18) HUMAN LYMPHOMAS - CLUSTERING AROUND JH ON CHROMOSOME-14 AND NEAR A TRANSCRIPTIONAL UNIT ON 18 [J].
BAKHSHI, A ;
JENSEN, JP ;
GOLDMAN, P ;
WRIGHT, JJ ;
MCBRIDE, OW ;
EPSTEIN, AL ;
KORSMEYER, SJ .
CELL, 1985, 41 (03) :899-906
[2]   Bax expression correlates with cellular drug sensitivity to doxorubicin, cyclophosphamide and chlorambucil but not fludarabine, cladribine or corticosteroids in B cell chronic lymphocytic leukemia [J].
Bosanquet, AG ;
Sturm, I ;
Wieder, T ;
Essmann, F ;
Bosanquet, MI ;
Head, FJ ;
Dörken, B ;
Daniel, PT .
LEUKEMIA, 2002, 16 (06) :1035-1044
[3]   Proapoptotic Bcl-2 relative bim required for certain apoptotic responses, leukocyte homeostasis, and to preclude autoimmunity [J].
Bouillet, P ;
Metcalf, D ;
Huang, DCS ;
Tarlinton, DM ;
Kay, TWH ;
Köntgen, F ;
Adams, JM ;
Strasser, A .
SCIENCE, 1999, 286 (5445) :1735-1738
[4]   BCL-X-L-regulated apoptosis in T cell development [J].
Chao, DT ;
Korsmeyer, SJ .
INTERNATIONAL IMMUNOLOGY, 1997, 9 (09) :1375-1384
[5]   BCL-2, BCL-XL sequester BH3 domain-only molecules preventing BAX- and BAK-mediated mitochondrial apoptosis [J].
Cheng, EHYA ;
Wei, MC ;
Weiler, S ;
Flavell, RA ;
Mak, TW ;
Lindsten, T ;
Korsmeyer, SJ .
MOLECULAR CELL, 2001, 8 (03) :705-711
[7]   Clinical relevance of BCL-2 overexpression in childhood acute lymphoblastic leukemia [J].
CoustanSmith, E ;
Kitanaka, A ;
Pui, CH ;
McNinch, L ;
Evans, WE ;
Raimondi, SC ;
Behm, FG ;
Arico, M ;
Campana, D .
BLOOD, 1996, 87 (03) :1140-1146
[8]   Cell death: Critical control points [J].
Danial, NN ;
Korsmeyer, SJ .
CELL, 2004, 116 (02) :205-219
[9]   BAD and glucokinase reside in a mitochondrial complex that integrates glycolysis and apoptosis [J].
Danial, NN ;
Gramm, CF ;
Scorrano, L ;
Zhang, CY ;
Krauss, S ;
Ranger, AM ;
Datta, SR ;
Greenberg, ME ;
Licklider, LJ ;
Lowell, BB ;
Gygi, SP ;
Korsmeyer, SJ .
NATURE, 2003, 424 (6951) :952-956
[10]   Survival factor-mediated BAD phosphorylation raises the mitochondrial threshold for apoptosis [J].
Datta, SR ;
Ranger, AM ;
Lin, MZ ;
Sturgill, JF ;
Ma, YC ;
Cowan, CW ;
Dikkes, P ;
Korsmeyer, SJ ;
Greenberg, ME .
DEVELOPMENTAL CELL, 2002, 3 (05) :631-643