Presensitization of human cells with extrinsic signals to induced chemical carcinogenesis.
Presensitization of human cells with extrinsic signals to induced chemical carcinogenesis.
复制标题
人类细胞对外在信号的预敏化诱导化学致癌作用。
DOI：
10.1002/ijc.2910260615
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发表时间：
1980
影响因子：
6.4
通讯作者：
DiPaolo,JA
中科院分区：
文献类型：
--
作者：
Milo,GE;DiPaolo,JA
当包皮衍生的低传代人类细胞群在G1期被阻断，从阻断中释放，并在细胞周期的S期用致癌物质N -甲基- N -硝基- N -亚硝基胍（MNNG）或黄曲霉毒素BI处理时，化学致癌物可重复转化。在g1期需要精氨酸和谷氨酰胺缺乏培养基来有效阻断细胞。S期早期，在致癌物前10 h加入雌二醇、胰岛素、炭疽素或肉豆酸酯佛波可使细胞群对致癌物治疗增敏。先敏化细胞在g1期阻滞48 h以上，在S期释放后用MNNG或黄曲霉毒素BI处理，未转化；在G2（4.5 h）、M （1.5 h）或G1（8.2 h）处理的现敏化细胞群中也没有发生转化。由经致癌物处理的现敏化细胞衍生的细胞在16 - 20 PDL的软琼脂中作为菌落生长。当从软琼脂中分离的菌落获得的细胞皮下注射到裸鼠体内时，肿瘤发生了。
Foreskin‐derived low‐passage human cell populations were reproducibly transformed with chemical carcinogens when the cells were blocked in G1, released from the block, and treated with either the carcinogenN‐methyl‐N‐nitro‐N‐nitrosoguanidine (MNNG) or with Aflatoxin BI in the S period of the cell cycle. Arginine‐and glutamine‐deficient medium was required to effectively block the cells in the G1period. Estradiol, insulin, anthralin or phorbol myristate acetate sensitized the cell population to carcinogen treatment when added 10 h before the carcinogen in early S period. Presensitized cells kept blocked in G1period for 48 h or longer, released and treated in S period with MNNG or Aflatoxin BI were not transformed; nor did transformation occur in presensitized cell populations treated in G2(4.5 h), M (1.5 h) or G1(8.2 h). Cells derived from carcinogen‐treated presensitized cells grew as colonies in soft agar at 16‐20 PDL. When cells derived from colonies isolated from the soft agar were injected subcutaneously into nude mice, tumors developed.