Non-homologous end joining mediated DNA repair is impaired in the NUP98-HOXD13 mouse model for myelodysplastic syndrome

被引：12
|
作者：
Puthiyaveetil, Abdul Gafoor [1 ]
Reilly, Christopher M. [2 ]
Pardee, Timothy S. [3 ]
Caudell, David L. [1 ]
机构：
[1] Virginia Tech, Lab Mol Pathol, Dept Biomed Sci & Pathobiol, Ctr Mol Med & Infect Dis, Blacksburg, VA 24061 USA
[2] Edward Via Virginia Coll Osteopath Med, Blacksburg, VA USA
[3] Wake Forest Univ Hlth Sci, Sect Hematol & Oncol, Dept Internal Med, Winston Salem, NC USA
来源：
LEUKEMIA RESEARCH | 2013年 / 37卷 / 01期
关键词：
Chromosomal translocation; NUP98; HOXD13; DNA double strand break; Non-homologous end joining; CLASS SWITCH RECOMBINATION; DOUBLE-STRAND BREAKS; GENOMIC INSTABILITY; CANCER; DAMAGE; MUTATIONS; MECHANISM; PROGNOSIS; LEUKEMIAS; PATHWAYS;
D O I：
10.1016/j.leukres.2012.10.012
中图分类号：
R73 [肿瘤学];
学科分类号：
100214 ;
摘要：
Chromosomal translocations typically impair cell differentiation and often require secondary mutations for malignant transformation. However, the role of a primary translocation in the development of collaborating mutations is debatable. To delineate the role of leukemic translocation NUP98-HOXD13 (NHD13) in secondary mutagenesis, DNA break and repair mechanisms in stimulated mouse B lymphocytes expressing NHD13 were analyzed. Our results showed significantly reduced expression of non-homologous end joining (NHEJ)-mediated DNA repair genes, DNA Pkcs, DNA ligase4, and Xrcc4 leading to cell cycle arrest at G2/M phase. Our results showed that expression of NHD13 fusion gene resulted in impaired NHEJ-mediated DNA break repair. (C) 2012 Elsevier Ltd. All rights reserved.
引用
收藏
页码：112 / 116
页数：5
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