Temporal sequence of mammary intraductal proliferations, ductal carcinomas in situ and adenocarcinomas induced by 1-methyl-1-nitrosourea in rats
Temporal sequence of mammary intraductal proliferations, ductal carcinomas in situ and adenocarcinomas induced by 1-methyl-1-nitrosourea in rats
复制标题
DOI：
10.1093/carcin/19.12.2181
复制
发表时间：
1998-12-01
期刊：
影响因子：
4.7
通讯作者：
Kelloff, GJ
中科院分区：
文献类型：
--
作者：
Thompson, HJ;McGinley, JN;Kelloff, GJ
乳腺癌发生的实验模型已被描述，其中导管内增生，导管原位癌和腺癌可以很容易地检测到，其发生的频率量化，在这项研究中报告的实验的目的是确定致癌剂管理和发生的每一个这些类型的病变之间的潜伏期。共150只雌性Sprague-Dawley大鼠在21日龄时腹腔注射50 mg 1-甲基-1-亚硝基脲（MNU）/kg体重。在致癌物后7、14、21、28和35天处死每组30只大鼠。乳腺导管内增生是第一个检测到的病变，并在致癌物给药后14天在20%的动物中观察到。在致癌物后21天，观察到原位导管癌和腺癌。每种类型的病变的数量随着致癌剂后的时间增加，但发生的时间模式是不同的病变类型。病变发生的模式是一致的导管内增殖是导管原位癌和腺癌的前驱病变，此外，数据表明，导管原位癌代表的形态进展的一个途径，导管内增殖演变为浸润性癌，但这种病变类型，目前定义的组织学，可能不是一个强制性的中间形态进展。这些发现与新出现的证据相一致，即多种但不同的致病途径导致乳腺癌，表现出不同的形态学模式和生物学活性。
An experimental model for mammary carcinogenesis has been described in which intraductal proliferations, ductal carcinomas in situ and adenocarcinomas can be readily detected and the frequency of their occurrence quantified, The objective of the experiment reported in this study was to determine the latency period between carcinogen administration and the occurrence of each of these types of lesion. A total of 150 female Sprague-Dawley rats were injected i.p. with 50 mg 1-methyl-1-nitrosourea (MNU)/kg body wt at 21 days of age. Groups of 30 rats each were killed at 7, 14, 21, 28 and 35 days post-carcinogen. Mammary intraductal proliferations were the first detected lesions and were observed in 20% of the animals at 14 days following carcinogen administration. At 21 days post-carcinogen ductal carcinomas in situ and adenocarcinomas were observed. The number of each type of lesion increased with time post-carcinogen, but the temporal pattern of occurrence was different among lesion types. The pattern of lesion occurrence was consistent with intraductal proliferations being a precursor lesion for ductal carcinomas in situ and adenocarcinomas, Furthermore, the data imply that ductal carcinomas in situ represent one pathway of morphological progression by which intraductal proliferations evolve into invasive carcinomas, but that this lesion type, as currently defined histologically, may not be an obligatory intermediate in morphologic progression. These findings are consistent with emerging evidence of multiple but distinct pathogenetic pathways leading to mammary carcinomas that display different morphological patterns and biological activities.