Nishiya I, Yoshizumi N, Fujiwara J, Kagabu T
Dept. of Obstetrics and Gynecology, School of Medicine, Iwate Medical University, Morioka.
Gan To Kagaku Ryoho. 1988 Oct;15(10):2871-81.
We investigated cisplatin resistant mechanisms in a cisplatin resistant ovarian cancer cell line (KFr) by means of flow cytometric analysis for damage of cisplatin to DNA base and DNA synthetic cells. Cisplatin showed cycle delay at 0.5 microgram/ml and then cycle arrest at 1 microgram/ml in G2 + M phase. KFr cells showed relatively rapid inhibition of DNA synthesis based with G-C base damage by cisplatin however, KFr cells had a capacity to repair DNA damage by cisplatin as showing cycle progression from G2 + M phase to G1-early S phase. Of the cisplatin derivatives tested which are of current clinical interest, Carboplatin and DWA 2114 R showed cross resistance to cisplatin in KFr cells.
我们通过流式细胞术分析顺铂对DNA碱基和DNA合成细胞的损伤,研究了顺铂耐药卵巢癌细胞系(KFr)中的顺铂耐药机制。顺铂在0.5微克/毫升时显示细胞周期延迟,然后在1微克/毫升时在G2+M期出现细胞周期停滞。KFr细胞显示出基于顺铂对G-C碱基损伤的相对快速的DNA合成抑制,然而,KFr细胞具有修复顺铂所致DNA损伤的能力,表现为从G2+M期到G1-早期S期的细胞周期进展。在所测试的具有当前临床意义的顺铂衍生物中,卡铂和DWA 2114 R在KFr细胞中显示出对顺铂的交叉耐药性。