Chromosomal translocations involving the MLL gene:: Molecular mechanisms

被引：46

作者：

Aplan, Peter D. ^{[1
]}

机构：

[1] NCI, Genet Branch,Ctr Canc Res, NIH, Natl Naval Med Ctr, Bethesda, MD 20889 USA

来源：

DNA REPAIR | 2006年 / 5卷 / 9-10期

关键词：

MLL; chromosomal translocation; infant leukemia; DNA topoisomerase II; non-homologous end joining;

D O I：

10.1016/j.dnarep.2006.05.034

中图分类号：

Q3 [遗传学];

学科分类号：

071007 ; 090102 ;

摘要：

A wide array of recurrent, non-random chromosomal translocations are associated with hematologic malignancies; experimental models have clearly demonstrated that many of these translocations are causal events during malignant transformation. Tyanslocations involving the MLL gene are among the most common of these non-random translocations. Leukemias with MLL translocations have been the topic of intense interest because of the unusual, biphenotypic immunophenotype of these leukemias, because of the unique clinical presentation of some MLL translocations (infant leukemia and therapy-related leukemia), and because of the large number of different chromosomal loci that partner with MLL in these translocations. This review is focused on the potential mechanisms that lead to MLL translocations, and will discuss aberrant VDJ recombination, Alv.-mediated recombination, non-homologous end joining, as well as the effect of DNA topoisomerase II poisons and chromatin structure. (c) 2006 Elsevier B.V. All rights reserved.

引用

页码：1265 / 1272

页数：8

共 73 条

[61] DNA cleavage within the MLL breakpoint cluster region is a specific event which occurs as part of higher-order chromatin fragmentation during the initial stages of apoptosis [J].

Stanulla, M ;

Wang, JJ ;

Chervinsky, DS ;

Thandla, S ;

Aplan, PD .

MOLECULAR AND CELLULAR BIOLOGY, 1997, 17 (07) :4070-4079

[62] Mechanisms of MLL gene rearrangement:: site-specific DNA cleavage within the breakpoint cluster region is independent of chromosomal context [J].

Stanulla, M ;

Chhalliyil, P ;

Wang, JJ ;

Jani-Sait, SN ;

Aplan, PD .

HUMAN MOLECULAR GENETICS, 2001, 10 (22) :2481-2491

[63] An in vivo topoisomerase II cleavage site and a DNase I hypersensitive site colocalize near exon 9 in the MLL breakpoint cluster region [J].

Strissel, PL ;

Strick, R ;

Rowley, JD ;

Zeleznik-Le, NJ .

BLOOD, 1998, 92 (10) :3793-3803

[64] The partial tandem duplication of ALL1 (MLL) is consistently generated by Alu-mediated homologous recombination in acute myeloid leukemia [J].

Strout, MP ;

Marcucci, G ;

Bloomfield, CD ;

Caligiuri, MA .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1998, 95 (05) :2390-2395

[65]

Super HG, 1997, GENE CHROMOSOME CANC, V20, P185, DOI 10.1002/(SICI)1098-2264(199710)20:2<185::AID-GCC9>3.0.CO

[66]

2-#

[67] REARRANGEMENT OF THE MLL GENE IN ACUTE LYMPHOBLASTIC AND ACUTE MYELOID LEUKEMIAS WITH 11Q23 CHROMOSOMAL TRANSLOCATIONS [J].

THIRMAN, MJ ;

GILL, HJ ;

BURNETT, RC ;

MBANGKOLLO, D ;

MCCABE, NR ;

KOBAYASHI, H ;

ZIEMINVANDERPOEL, S ;

KANEKO, Y ;

MORGAN, R ;

SANDBERG, AA ;

CHAGANTI, RSK ;

LARSON, RA ;

LEBEAU, MM ;

DIAZ, MO ;

ROWLEY, JD .

NEW ENGLAND JOURNAL OF MEDICINE, 1993, 329 (13) :909-914

[68]

TYCKO B, 1990, CANCER CELL-MON REV, V2, P1

[69] Surviving apoptosis [J].

Vaughan, ATM ;

Betti, CJ ;

Villalobos, MJ .

APOPTOSIS, 2002, 7 (02) :173-177

[70] Reciprocal DNA topoisomerase II cleavage events at 5′-TATTA-3′ sequences in MLL and AF-9 create homologous single-stranded overhangs that anneal to form der(11) and der(9) genomic breakpoint junctions in treatment-related AML without further processing [J].

Whitmarsh, RJ ;

Saginario, C ;

Zhuo, Y ;

Hilgenfeld, E ;

Rappaport, EF ;

Megonigal, MD ;

Carroll, M ;

Liu, M ;

Osheroff, N ;

Cheung, NKV ;

Slater, DJ ;

Ried, T ;

Knutsen, T ;

Blair, IA ;

Felix, CA .

ONCOGENE, 2003, 22 (52) :8448-8459

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