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

页码：112 / 116

页数：5

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