Origin of Chromosomal Translocations in Lymphoid Cancer

被引：230

作者：

Nussenzweig, Andre ^{[1
]}

Nussenzweig, Michel C. ^{[2
,3
]}

机构：

[1] NCI, Expt Immunol Branch, NIH, Bethesda, MD 20892 USA

[2] Rockefeller Univ, Labs Mol Immunol, New York, NY 10065 USA

[3] Howard Hughes Med Inst, Chevy Chase, MD 20815 USA

来源：

CELL | 2010年 / 141卷 / 01期

基金：

美国国家卫生研究院;

关键词：

CLASS-SWITCH RECOMBINATION; DOUBLE-STRAND BREAKS; INDUCED CYTIDINE DEAMINASE; END-JOINING PATHWAY; B-CELL LYMPHOMA; SOMATIC HYPERMUTATION; V(D)J RECOMBINATION; DNA-REPAIR; MAMMALIAN-CELLS; GENOMIC INSTABILITY;

D O I：

10.1016/j.cell.2010.03.016

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Aberrant fusions between heterologous chromosomes are among the most prevalent cytogenetic abnormalities found in cancer cells. Oncogenic chromosomal translocations provide cells with a proliferative or survival advantage. They may either initiate transformation or be acquired secondarily as a result of genomic instability. Here, we highlight recent advances toward understanding the origin of chromosomal translocations in incipient lymphoid cancers and how tumor-suppressive pathways normally limit the frequency of these aberrant recombination events. Deciphering the mechanisms that mediate chromosomal fusions will open new avenues for developing therapeutic strategies aimed at eliminating lesions that lead to the initiation, maintenance, and progression of cancer.

引用

页码：27 / 38

页数：12

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