DBA/2 MICE ARE AS SENSITIVE AS SENCAR MICE TO SKIN TUMOR PROMOTION BY 12-0-TETRADECANOYLPHORBOL-13-ACETATE
DBA/2 MICE ARE AS SENSITIVE AS SENCAR MICE TO SKIN TUMOR PROMOTION BY 12-0-TETRADECANOYLPHORBOL-13-ACETATE
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DOI：
10.1093/carcin/5.11.1493
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发表时间：
1984-01-01
期刊：
影响因子：
4.7
通讯作者：
DIAMOND, L
中科院分区：
文献类型：
--
作者：
DIGIOVANNI, J;PRICHETT, WP;DIAMOND, L
当使用高起始剂量（400 nmol/小鼠）的7，12-二甲基苯并[a]蒽时，近交系DBA/2小鼠对2阶段起始-促进肿瘤发生方案有反应。当用N-甲基-N“-硝基-N-亚硝基胍（MNNG）作引发剂时，它们也有反应。在这两种情况下的肿瘤反应的特点是快速的肿瘤发展速度与最大的肿瘤反应达到第15周或之前的促进与12-O-十四酰基佛波醇-13-乙酸酯（TPA）。当DBA/2小鼠与SENCAR小鼠比较MNNG启动后的促进敏感性时，2只小鼠原种的肿瘤反应几乎相同。C57 BL/6小鼠基本上对TPA促进具有抗性，而与所使用的引发剂或引发剂的剂量无关。进行了初步研究，以确定如何在DBA/2（敏感）和C57 BL/6（耐药）亲本衍生的F1小鼠中遗传TPA促进肿瘤的易感性。B6 D2 F1小鼠与DBA/2亲本一样敏感，表明这2个近交系小鼠品系的易感性以常染色体显性性状遗传。这2个近交系小鼠可能为研究遗传因素控制佛波酯皮肤肿瘤促进的易感性提供了模型系统。
Mice of the inbred strain DBA/2 responded to a 2-stage, initiation-promotion tumorigenesis protocol when high initiating doses (400 nmol/mouse) of 7,12-dimethylbenz[a]anthracene were utilized. They also responded when N-methyl-N''-nitro-N-nitrosoguanidine (MNNG) was used as the initiating agent. The tumor response in both cases was characterized by a rapid rate of tumor development with the maximal tumor responses reached on or before the 15th wk of promotion with 12-O-tetradecanoylphorbol-13-acetate (TPA). When DBA/2 mice were compared with SENCAR mice for promotion sensitivity following initiation with MNNG, the 2 mouse stocks responded with a nearly identical tumor response. C57BL/6 mice were essentially resistant to TPA promotion regardless of the initiator or the dose of initiator used. A preliminary study was conducted to determine how susceptibility to tumor promotion by TPA was inherited in F1 mice derived from DBA/2 (sensitive) and C57BL/6 (resistant) parents. The B6D2F1 mice were as sensitive as the DBA/2 parent, suggesting that susceptibility in these 2 inbred mouse strains is inherited as an autosomal dominant trait. These 2 inbred mouse strains may provide a model system for studying genetic factors controlling susceptibility to phorbol ester skin tumor promotion.