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D1小鼠乳腺增生性瘤株的一个高肿瘤发生率亚系:致癌物的作用。

A high-tumor-incidence subline of the D1 mouse mammary hyperplastic outgrowth line: effect of carcinogens.

作者信息

Ashley R L, Cardiff R D, Pratt T S, Faulkin L J

出版信息

J Natl Cancer Inst. 1982 Sep;69(3):639-45.

PMID:6287083
Abstract

Mammary tumorigenesis in some mouse strains is characterized by the appearance of a preneoplastic lesion, the hyperplastic alveolar nodule (HAN). The biology of the HAN has been characterized primarily through the study of stable outgrowth lines of serially transplanted HAN. One outgrowth line, Dl, which was developed and carried in female BALB/c mice, has been described as a low-tumor-incidence line that does not express murine mammary tumor virus (MuMTV) and is susceptible to hormonal, chemical, and viral carcinogens. In this report, a high-tumor-incidence subline of Dl, Dl/UCD, is described. Although Dl/UCD, like Dl, is susceptible to the chemical carcinogen 7,12-dimethylbenz[a]anthracene, an increase in tumor incidence was not observed when Dl/UCD outgrowth was exposed to hormones by means of pituitary isografts. Unlike Dl, Dl/UCD is refractory to the carcinogenic action of MuMTV. Both Dl and the Dl/UCD subline contained the endogenous MuMTV provirus but did not contain exogenous MuMTV provirus sequences. MuMTV antigen was not detected in Dl/UCD outgrowths or tumors. RNA hybridizable to MuMTV complementary DNA was detected in some Dl/UCD outgrowths and tumors but did not appear to correlate with tumorigenesis.

摘要

某些小鼠品系的乳腺肿瘤发生以一种癌前病变即增生性肺泡结节(HAN)的出现为特征。HAN的生物学特性主要是通过对连续移植的HAN稳定传代系的研究来表征的。一个传代系Dl,是在雌性BALB/c小鼠中培育并传代的,被描述为低肿瘤发生率品系,不表达鼠乳腺肿瘤病毒(MuMTV),且对激素、化学和病毒致癌物敏感。在本报告中,描述了Dl的一个高肿瘤发生率亚系Dl/UCD。尽管Dl/UCD与Dl一样对化学致癌物7,12 - 二甲基苯并[a]蒽敏感,但当通过垂体同基因移植使Dl/UCD传代系接触激素时,未观察到肿瘤发生率增加。与Dl不同,Dl/UCD对MuMTV的致癌作用具有抗性。Dl和Dl/UCD亚系均含有内源性MuMTV前病毒,但不含有外源性MuMTV前病毒序列。在Dl/UCD传代系或肿瘤中未检测到MuMTV抗原。在一些Dl/UCD传代系和肿瘤中检测到了可与MuMTV互补DNA杂交的RNA,但这似乎与肿瘤发生无关。

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A high-tumor-incidence subline of the D1 mouse mammary hyperplastic outgrowth line: effect of carcinogens.D1小鼠乳腺增生性瘤株的一个高肿瘤发生率亚系:致癌物的作用。
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