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
[31]   Double-strand breaks and translocations in cancer [J].
Elliott, B ;
Jasin, M .
CELLULAR AND MOLECULAR LIFE SCIENCES, 2002, 59 (02) :373-385
[32]   Secondary leukemias induced by topoisomerase-targeted drugs [J].
Felix, CA .
BIOCHIMICA ET BIOPHYSICA ACTA-GENE STRUCTURE AND EXPRESSION, 1998, 1400 (1-3) :233-255
[33]   Structure, function and DNA composition of Saccharomyces cerevisiae chromatin loops [J].
Filipski, J ;
Mucha, M .
GENE, 2002, 300 (1-2) :63-68
[34]   Topoisomerase II as a target for anticancer drugs: When enzymes stop being nice [J].
Fortune, JM ;
Osheroff, N .
PROGRESS IN NUCLEIC ACID RESEARCH AND MOLECULAR BIOLOGY, VOL 64, 2000, 64 :221-253
[35]  
GALE KC, 1992, J BIOL CHEM, V267, P12090
[36]   FUSION OF PDGF RECEPTOR-BETA TO A NOVEL ETS-LIKE GENE, TEL, IN CHRONIC MYELOMONOCYTIC LEUKEMIA WITH T(512) CHROMOSOMAL TRANSLOCATION [J].
GOLUB, TR ;
BARKER, GF ;
LOVETT, M ;
GILLILAND, DG .
CELL, 1994, 77 (02) :307-316
[37]  
Hart SM, 2002, HAEMATOLOGICA, V87, P1307
[38]   Better use of Darwinian concepts might change the way we look at some diseases [J].
Hayward, DA .
MEDICAL HYPOTHESES, 2000, 54 (06) :895-899
[39]   Breakpoints of t(4;11) translocations in the human MLL and AF4 genes in all patients are preferentially clustered outside of high-affinity matrix attachment regions [J].
Hensel, JP ;
Gillert, E ;
Fey, GH ;
Marschalek, R .
JOURNAL OF CELLULAR BIOCHEMISTRY, 2001, 82 (02) :299-309
[40]   Translin binds to the sequences adjacent to the breakpoints of the TLS and CHOP genes in liposarcomas with translocation t(12;16) [J].
Hosaka, T ;
Kanoe, H ;
Nakayama, T ;
Murakami, H ;
Yamamoto, H ;
Nakamata, T ;
Tsuboyama, T ;
Oka, M ;
Kasai, M ;
Sasaki, MS ;
Nakamura, T ;
Toguchida, J .
ONCOGENE, 2000, 19 (50) :5821-5825