Topoisomerase II and the etiology of chromosomal translocations

被引：110

作者：

Felix, Carolyn A.

Kolaris, Christos P.

Osheroff, Neil

机构：

[1] Childrens Hosp Philadelphia, Leonard & Madlyn Abramson Pediat Res Ctr, Div Oncol, Philadelphia, PA 19104 USA

[2] Univ Penn, Sch Med, Dept Pediat, Philadelphia, PA 19104 USA

[3] Vanderbilt Univ, Sch Med, Dept Biochem, Nashville, TN 37232 USA

[4] Vanderbilt Univ, Sch Med, Dept Med Hematol Oncol, Nashville, TN 37232 USA

来源：

DNA REPAIR | 2006年 / 5卷 / 9-10期

关键词：

leukemia; epipodophyllotoxin; topoisomerase II; translocation; MLL gene;

D O I：

10.1016/j.dnarep.2006.05.031

中图分类号：

Q3 [遗传学];

学科分类号：

071007 ; 090102 ;

摘要：

Acute leukemias with balanced chromosomal translocations, protean morphologic and immunophenotypic presentations but generally shorter latency and absence of myelodysplasia are recognized as a complication of anti-cancer drugs that behave as topoisomerase II poisons. Translocations affecting the breakpoint cluster region of the MLL gene at chromosome band 11q23 are the most common molecular genetic: aberrations in leukemias associated with the topoisomerase II poisons. These agents perturb the cleavage-religation equilibrium of topoisomerase II and increase cleavage complexes. One model suggests that this damages the DNA directly and leads to chromosomal breakage, which may result in untoward DNA recombination in the form of translocations. This review will summarize the evidence for topoisomerase II involvement in the genesis of translocations and extension of the model to acute leukemia in infants characterized by similar MLL translocations. (c) 2006 Elsevier B.V. All rights reserved.

引用

页码：1093 / 1108

页数：16

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