Damage-resistant DNA synthesis in Fanconi anemia cells treated with a DNA gross-linking agent
Damage-resistant DNA synthesis in Fanconi anemia cells treated with a DNA gross-linking agent
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DOI：
10.1006/excr.2000.4995
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发表时间：
2000-11-01
影响因子：
3.7
通讯作者：
Lambert, WC
中科院分区：
文献类型：
--
作者：
Centurion, SA;Kuo, HR;Lambert, WC
范可尼贫血（FA）是一种隐性疾病，与各种先天性异常，进行性骨髓衰竭，并有显着的倾向，发展为癌症。在细胞水平上，FA的特征是增殖细胞的G（2）期延长，并且对产生DNA链间交联的试剂的细胞毒性和致染色体断裂作用具有明显的超敏反应。用这些试剂处理导致FA细胞中G（2）期甚至进一步延长。我们现在表明，FA细胞，从四个不同的互补组，不能降低其复制DNA合成的速率，正常细胞一样，用DNA交联剂治疗后。这可能是导致这些细胞中G2期延长的原因，并表明FA细胞对DNA交联剂反应的根本缺陷可能是在细胞周期的S期，而不是G（2）期。(C)北京大学出版社.
Fanconi anemia (FA) is a recessive disorder associated with diverse congenital anomalies, progressive bone marrow failure, and a marked predisposition to develop cancer. At the cellular level, FA is characterized by a prolonged G(2) phase in proliferating cells and a marked hypersensitivity to both the cytotoxic and the clastogenic effects of agents which produce DNA interstrand cross-links. Treatment with these agents leads to even further prolongation of the G(2) phase in FA cells. We now show that FA cells, from four different complementation groups, fail to decrease their rates of replicative DNA synthesis, as do normal cells, following treatment with a DNA cross-linking agent. This may be responsible for the prolongation of the G2 phase seen in these cells, and suggests that the fundamental defect in response of FA cells to DNA crosslinking agents may be in the S phase, rather than the G(2) phase, of the cell cycle. (C) 2000 Academic Press.