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阿霉素处理后L929细胞的DNA合成。

DNA synthesis by L929 cells following doxorubicin exposure.

作者信息

Lanks K W, Lehman J M

机构信息

Department of Pathology, State University of New York, Health Science Center, Brooklyn 11203-2098.

出版信息

Cancer Res. 1990 Aug 1;50(15):4776-8.

PMID:2369751
Abstract

Doxorubicin does not kill L929 cells at concentrations that profoundly reduce clonogenic survival. Instead, the cell and nuclear volume progressively increase for at least 1 week following drug exposure leading to the production of characteristic giant cells. The increase in nuclear volume is due to continued DNA synthesis and increase in chromosome number without entry into mitosis. The implications of this finding for in vitro chemosensitivity assays and for the mechanism of doxorubicin cytotoxicity are discussed.

摘要

阿霉素在能显著降低克隆形成存活率的浓度下并不会杀死L929细胞。相反,在药物暴露后的至少1周内,细胞和细胞核体积会逐渐增大,导致特征性巨细胞的产生。细胞核体积的增大是由于DNA持续合成以及染色体数目增加,但细胞并未进入有丝分裂。本文讨论了这一发现对体外化学敏感性测定以及阿霉素细胞毒性机制的影响。

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DNA synthesis by L929 cells following doxorubicin exposure.阿霉素处理后L929细胞的DNA合成。
Cancer Res. 1990 Aug 1;50(15):4776-8.
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Lack of synchrony among multiple nuclei induces partial DNA fragmentation in V79 cells polyploidized by demecolcine.多个细胞核之间缺乏同步性会导致秋水仙胺诱导多倍体化的V79细胞中出现部分DNA片段化。
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