Nexø B A, Ulrich K
Cancer Res. 1978 Mar;38(3):729-35.
Repeated percutaneous applications of 7,12-dimethylbenz(a)anthracene on weaning DBA/2 and ST/a mice induced 100% leukemias with short latency periods. Endogenous C-type viruses were activated during the treatment as evidenced by (a) increased expression of the murine leukemia virus major core protein, p30, in blood and spleens and (b) increased frequency of detection of ecotropic virus by cocultivation of the splenocytes with SC-1 cells. The treatment did not affect p30 expression in several nonlymphoid organs, and detection of xenotropic viruses in the splenocytes was decreased. Virus expression did not correlate with the progression of disease in that (a) high p30 levels were generally found in mice with relatively low spleen weights and (b) p30 levels had no obvious connection to survival of the individual. 7,12-Dimethylbenz(a)anthracene treatment had little influence on p30 expression in spleens and blood from C3H and BALB/c mice, which are less sensitive to 7,12-dimethylbenz(a)anthracene-induced leukemogenesis. The results indicate an association of C-type virus activation with chemical induction of leukemia but do not necessarily imply an etiological role of the virus in the disease.
在断奶的DBA/2和ST/a小鼠身上反复经皮涂抹7,12-二甲基苯并(a)蒽可在短潜伏期内诱发100%的白血病。治疗期间内源性C型病毒被激活，证据如下：(a) 血液和脾脏中鼠白血病病毒主要核心蛋白p30的表达增加；(b) 通过脾细胞与SC-1细胞共培养，嗜亲性病毒的检测频率增加。该治疗不影响几种非淋巴器官中的p30表达，且脾细胞中异嗜性病毒的检测率降低。病毒表达与疾病进展无关，因为：(a) p30水平通常在脾脏重量相对较低的小鼠中较高；(b) p30水平与个体存活无明显关联。7,12-二甲基苯并(a)蒽处理对C3H和BALB/c小鼠脾脏和血液中的p30表达影响很小，这两种小鼠对7,12-二甲基苯并(a)蒽诱导的白血病发生不太敏感。结果表明C型病毒激活与白血病的化学诱导有关，但不一定意味着病毒在该疾病中具有病因学作用。
