Breakpoint clusters: Reason or consequence?

被引:22
作者
Bystritskiy, AA [1 ]
Razin, SV [1 ]
机构
[1] Russian Acad Sci, Inst Gene Biol, Lab Struct & Funct Org Chromosomes, Moscow 119334, Russia
来源
CRITICAL REVIEWS IN EUKARYOTIC GENE EXPRESSION | 2004年 / 14卷 / 1-2期
关键词
cancer; chromosomal rearrangements; double-strand breaks; nuclear architecture; protein domains; natural selection;
D O I
10.1615/CritRevEukaryotGeneExpr.v14.i12.40
中图分类号
Q81 [生物工程学(生物技术)]; Q93 [微生物学];
学科分类号
071005 ; 0836 ; 090102 ; 100705 ;
摘要
Chromosomal rearrangements are common causes of cancer. In the majority of cases, the malignancy is induced via an altered transcription factor. The breakpoints of such translocations are often mysteriously tightly clustered in the genome. Even more surprisingly, such breakpoint dusters often contain specific genomic elements, such as topoisomerase II consensus sites, nuclear matrix attachment regions, etc. In this review, we discuss the common idea of breakpoints being induced by chromatin structure. We also touch on the question of whether the structure of corresponding proteins is related to the positions of breakpoints. Finally, we refer to recent works on chromosome territories and their distribution in the interphase nucleus.
引用
收藏
页码:65 / 77
页数:13
相关论文
共 114 条
[51]   Molecular analysis of new subtypes of ELE/RET rearrangements, their reciprocal transcripts and breakpoints in papillary thyroid carcinomas of children after Chernobyl [J].
Klugbauer, S ;
Demidchik, EP ;
Lengfelder, E ;
Rabes, HM .
ONCOGENE, 1998, 16 (05) :671-675
[52]   Loss of androgen receptor associated protein 70 (ARA70) expression in a subset of HER2-positive breast cancers [J].
Kollara, A ;
Kahn, HJ ;
Marks, A ;
Brown, TJ .
BREAST CANCER RESEARCH AND TREATMENT, 2001, 67 (03) :245-253
[53]   3D Structure of the human genome:: order in randomness [J].
Kozubek, S ;
Lukásová, E ;
Jirsová, P ;
Koutná, I ;
Kozubek, M ;
Ganová, A ;
Bártová, E ;
Falk, M ;
Paseková, R .
CHROMOSOMA, 2002, 111 (05) :321-331
[54]   The topological organization of chromosomes 9 and 22 in cell nuclei has a determinative role in the induction of t(9,22) translocations and in the pathogenesis of t(9,22) leukemias [J].
Kozubek, S ;
Lukásová, E ;
Marecková, A ;
Skalníková, M ;
Kozubek, M ;
Bártová, E ;
Kroha, V ;
Krahulcová, E ;
Slotová, J .
CHROMOSOMA, 1999, 108 (07) :426-435
[55]  
Kulkarni S, 2000, CANCER RES, V60, P3592
[56]   Therapy related leukemias: Susceptibility, prevention and treatment [J].
Leone, G ;
Voso, MT ;
Sica, S ;
Morosetti, R ;
Pagano, L .
LEUKEMIA & LYMPHOMA, 2001, 41 (3-4) :255-276
[57]  
Liu J, 2000, CLIN CANCER RES, V6, P3522
[58]   Rabaptin-5 is a novel fusion partner to platelet-derived growth factor β receptor in chronic myelomonocytic leukemia [J].
Magnusson, MK ;
Meade, KE ;
Brown, KE ;
Arthur, DC ;
Krueger, LA ;
Barrett, AJ ;
Dunbar, CE .
BLOOD, 2001, 98 (08) :2518-2525
[59]   The structure of the human ALL-1/MLL/HRX gene [J].
Marschalek, R ;
Nilson, I ;
Löchner, K ;
Greim, R ;
Siegler, G ;
Greil, J ;
Beck, JD ;
Fey, GH .
LEUKEMIA & LYMPHOMA, 1997, 27 (5-6) :417-+
[60]   Recurrent chromosome aberrations in cancer [J].
Mitelman, F .
MUTATION RESEARCH-REVIEWS IN MUTATION RESEARCH, 2000, 462 (2-3) :247-253