共查询到20条相似文献,搜索用时 31 毫秒
1.
2.
Nucleotide excision repair in rat male germ cells: low level of repair in intact cells contrasts with high dual incision activity in vitro 总被引:1,自引:0,他引:1 下载免费PDF全文
Jansen J Olsen AK Wiger R Naegeli H de Boer P van Der Hoeven F Holme JA Brunborg G Mullenders L 《Nucleic acids research》2001,29(8):1791-1800
3.
4.
5.
6.
7.
8.
《Cell cycle (Georgetown, Tex.)》2013,12(14):2276-2280
Different mechanisms account for the development of B lymphoma. Malignant transformation of B lymphocytes arises from progressive loss of genome integrity combined with uncontrolled cell proliferation, often triggered by foreign or self antigens. It is well established that somatic hypermutation, the pathway responsible for introducing high levels of mutations in immunoglobulin genes, also targets several other genes, contributing mainly to germinal center-derived B-cell lymphoma. We have recently discovered that a major DNA repair pathway, nucleotide excision repair (NER), is downregulated in quiescent B lymphocytes. Upon B-cell stimulation, unrepaired DNA damage results in the accumulation of mutations in a different and likely larger set of genes, including normally silent genes (e.g., oncogenes) as well as cell cycle and activation-induced genes. This mechanism potentially produces a transforming event relevant to a wider palette of B lymphomas. Here we discuss the relative contribution of both mechanisms to lymphomagenesis and possible implications of NER downregulation for other types of malignancies and for B cell-mediated immunity. Given that hematopoietic cancer stem cells remain quiescent for long periods of time, we propose that downregulation of NER during quiescence, in an environment that causes both genotoxic stress and proliferation, could be a general mechanism for carcinogenesis. 相似文献
9.
10.
Kobayashi K O'Driscoll M Macpherson P Mullenders L Vreeswijk M Karran P 《DNA Repair》2004,3(6):649-657
11.
12.
13.
14.
15.
16.
17.
18.
19.