Dzarlieva R T, Fusenig N E
Cancer Lett. 1982 May-Jun;16(1):7-17. doi: 10.1016/0304-3835(82)90085-4.
The tumor 12-O-tetradecanoyl-phorbol-13-acetate (TPA) moderately stimulated sister chromatid exchanges in primary epidermal cultures (PEC) from C3H mice, and strongly enhanced structural chromosome aberrations. In G-banded metaphases for TPA (10-(8) and 10-(6) M for 54 h) treated PEC aneuploidy (hypo- and hyperdiploidy) increased and structural aberrations were enhanced 8- to 10-fold. Breaks, fragments and metacentric chromosomes had raised 7- to 11-fold. Chromatid interchanges (tri- and quadri-radials) and centromeric splitting, virtually absent in controls, appeared in 4--8% of metaphases. The non-promoting 4-O-methyl-TPA did not induce chromosomal alterations. These substantial effects on the genetic material of target cells represent a new aspect of the mechanism of action of tumor-promoting phorbol esters.
肿瘤促进剂12 - O -十四烷酰佛波醇-13 -乙酸酯（TPA）适度刺激了C3H小鼠原代表皮培养物（PEC）中的姐妹染色单体交换，并强烈增强了染色体结构畸变。在经TPA（10⁻⁸和10⁻⁶M处理54小时）处理的PEC的G带中期相中，非整倍体（亚二倍体和超二倍体）增加，结构畸变增强了8至10倍。断裂、片段和中着丝粒染色体增加了7至11倍。对照中几乎不存在的染色单体互换（三价和四价体）和着丝粒分裂出现在4%至8%的中期相中。无促进作用的4 - O -甲基TPA不诱导染色体改变。这些对靶细胞遗传物质的显著影响代表了肿瘤促进佛波酯作用机制的一个新方面。
