Molecular biology of Burkitt's lymphoma

被引:273
作者
Hecht, JL
Aster, JC
机构
[1] Brigham & Womens Hosp, Dept Pathol, Boston, MA 02115 USA
[2] Harvard Univ, Sch Med, Dept Pathol, Boston, MA 02115 USA
关键词
D O I
10.1200/JCO.2000.18.21.3707
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
The diagnostic category of Burkitt's lymphoma encompasses a closely related group of aggressive B-cell tumors that includes sporadic, endemic, and human immunodeficiency virus-associated subtypes. All subtypes are characterized by chromosomal rearrangements involving the c-myc proto-oncogene that lead to its inappropriate expression. This review focuses on the roles of c-myc dysregulation and EpsreinBarr virus infection in Burkitt's lymphoma. Although the normal function of c-myc remains enigmatic, recent data indicate that it has a central role in several fundamental aspects of cellular biology, including proliferation, differentiation, metabolism, apoptosis, and telomere maintenance. We discuss new insights into the molecular mechanisms of these c-Myc activities and their potential relevance to the pathogenesis of Burkitt's lymphoma and speculate on the role of EpsteinBarr virus. (C) 2000 by American Society of Clinical Oncology.
引用
收藏
页码:3707 / 3721
页数:15
相关论文
共 153 条
[1]   Molecular and clinical features of non-Burkitt's, diffuse large-cell lymphoma of B-cell type associated with the c-MYC/immunoglobulin heavy-chain fusion gene [J].
Akasaka, T ;
Akasaka, H ;
Ueda, C ;
Yonetani, N ;
Maesako, Y ;
Shimizu, A ;
Yamabe, H ;
Fukuhara, S ;
Uchiyama, T ;
Ohno, H .
JOURNAL OF CLINICAL ONCOLOGY, 2000, 18 (03) :510-518
[2]   Distinct types of diffuse large B-cell lymphoma identified by gene expression profiling [J].
Alizadeh, AA ;
Eisen, MB ;
Davis, RE ;
Ma, C ;
Lossos, IS ;
Rosenwald, A ;
Boldrick, JG ;
Sabet, H ;
Tran, T ;
Yu, X ;
Powell, JI ;
Yang, LM ;
Marti, GE ;
Moore, T ;
Hudson, J ;
Lu, LS ;
Lewis, DB ;
Tibshirani, R ;
Sherlock, G ;
Chan, WC ;
Greiner, TC ;
Weisenburger, DD ;
Armitage, JO ;
Warnke, R ;
Levy, R ;
Wilson, W ;
Grever, MR ;
Byrd, JC ;
Botstein, D ;
Brown, PO ;
Staudt, LM .
NATURE, 2000, 403 (6769) :503-511
[3]   Role for N-CoR and histone deacetylase in Sin3-mediated transcriptional repression [J].
Alland, L ;
Muhle, R ;
Hou, H ;
Potes, J ;
Chin, L ;
SchreiberAgus, N ;
DePinho, RA .
NATURE, 1997, 387 (6628) :49-55
[4]   ONCOGENIC ACTIVITY OF THE C-MYC PROTEIN REQUIRES DIMERIZATION WITH MAX [J].
AMATI, B ;
BROOKS, MW ;
LEVY, N ;
LITTLEWOOD, TD ;
EVAN, GI ;
LAND, H .
CELL, 1993, 72 (02) :233-245
[5]   TRANSCRIPTIONAL ACTIVATION BY THE HUMAN C-MYC ONCOPROTEIN IN YEAST REQUIRES INTERACTION WITH MAX [J].
AMATI, B ;
DALTON, S ;
BROOKS, MW ;
LITTLEWOOD, TD ;
EVAN, GI ;
LAND, H .
NATURE, 1992, 359 (6394) :423-426
[6]   DIFFERENTIAL EXPRESSION OF THE TRANSLOCATED AND THE UNTRANSLOCATED C-MYC ONCOGENE IN BURKITT-LYMPHOMA [J].
ARRUSHDI, A ;
NISHIKURA, K ;
ERIKSON, J ;
WATT, R ;
ROVERA, G ;
CROCE, CM .
SCIENCE, 1983, 222 (4622) :390-393
[7]   MAD - A HETERODIMERIC PARTNER FOR MAX THAT ANTAGONIZES MYC TRANSCRIPTIONAL ACTIVITY [J].
AYER, DE ;
KRETZNER, L ;
EISENMAN, RN .
CELL, 1993, 72 (02) :211-222
[8]   c-Myc hot spot mutations in lymphomas result in inefficient ubiquitination and decreased proteasome-mediated turnover [J].
Bahram, F ;
von der Lehr, N ;
Cetinkaya, C ;
Larsson, LG .
BLOOD, 2000, 95 (06) :2104-2110
[9]   THE ORNITHINE DECARBOXYLASE GENE IS A TRANSCRIPTIONAL TARGET OF C-MYC [J].
BELLOFERNANDEZ, C ;
PACKHAM, G ;
CLEVELAND, JL .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1993, 90 (16) :7804-7808
[10]   A BLOCK TO ELONGATION IS LARGELY RESPONSIBLE FOR DECREASED TRANSCRIPTION OF C-MYC IN DIFFERENTIATED HL60 CELLS [J].
BENTLEY, DL ;
GROUDINE, M .
NATURE, 1986, 321 (6071) :702-706