Centurion S A, Kuo H R, Lambert W C
Department of Pathology and Laboratory Medicine, UMDNJ-New Jersey Medical School, Newark, New Jersey, 07103-2714, USA.
Exp Cell Res. 2000 Nov 1;260(2):216-21. doi: 10.1006/excr.2000.4995.
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 cross-linking agents may be in the S phase, rather than the G(2) phase, of the cell cycle.
范可尼贫血（FA）是一种隐性疾病，与多种先天性异常、进行性骨髓衰竭以及患癌的显著倾向相关。在细胞水平上，FA的特征是增殖细胞中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断裂效应具有明显的超敏感性。用这些试剂处理会导致FA细胞中G(2)期进一步延长。我们现在表明，来自四个不同互补组的FA细胞在经DNA交联剂处理后，无法像正常细胞那样降低其复制性DNA合成速率。这可能是这些细胞中所见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在细胞周期的S期，而非G(2)期。
