Fischer S M, Conti C J, Locniskar M, Belury M A, Maldve R E, Lee M L, Leyton J, Slaga T J, Bechtel D H
University of Texas M. D. Anderson Cancer Center, Science Park Research Division, Smithville 78957.
Cancer Res. 1992 Feb 1;52(3):662-6.
We recently reported (J. Leyton et al., Cancer Res., 51: 907-915, 1991) an inverse correlation between skin tumor number and level of dietary linoleic acid (LA) in SENCAR mice following an initiation-promotion protocol. These results differed from the reported (C. Ip et al., Cancer Res., 45: 1997-2001, 1985) positive correlation between dietary LA and tumor incidence for the rat mammary gland. The goal of the study reported here was to determine whether this dissimilarity was due to organ site or species differences. Female SENCAR mice were fed 1 of 3 15% fat diets containing LA at levels of 0.8, 4.5, and 8.4% before, during, and after intragastric administration of 6 mg (1 mg/week) 7,12-dimethylbenz(a)anthracene. A positive correlation between level of dietary LA and mammary tumor incidence was observed such that for the first 15 weeks, the incidence was greatest in the 8.4% LA diet group, followed by the 4.5% and then the 0.8% LA groups. Distinct dietary effects on latency were also noted in that 15, 12, and 8 weeks after cessation of 7,12-dimethylbenz(a)anthracene were required for a 40% carcinoma incidence in the 0.8, 4.5, and 8.4% LA diet groups, respectively. A histopathological analysis of all tumors revealed that the predominant type was the adenosquamous carcinoma, which comprised 46.6, 54.1, and 77.7% of all mammary tumors for diets containing 0.8, 4.5, and 8.4% LA, respectively. The second most common tumor was the adenocarcinoma type B, which was found with a frequency of 33% in the 0.8% and 4.5% LA diet groups and 22% in the 8.4% LA diet group. These results indicate that SENCAR mice have a short latency period for 7,12-dimethylbenz(a)anthracene-induced mammary tumor development and that rat and mouse mammary tumor development is modified by dietary LA in a similar manner, although in the SENCAR mouse dietary LA did not have a saturating effect. In addition, high dietary LA was found to be associated specifically with an increased incidence of adenosquamous carcinomas but not of other types of mammary tumors.
我们最近报道了（J. Leyton等人，《癌症研究》，51: 907 - 915, 1991），在启动 - 促癌实验方案下，SENCAR小鼠的皮肤肿瘤数量与膳食亚油酸（LA）水平呈负相关。这些结果与报道的（C. Ip等人，《癌症研究》，45: 1997 - 2001, 1985）大鼠乳腺中膳食LA与肿瘤发生率的正相关不同。本研究的目的是确定这种差异是由于器官部位还是物种差异所致。给雌性SENCAR小鼠喂食三种含15%脂肪的日粮中的一种，其中LA水平分别为0.8%、4.5%和8.4%，在胃内给予6毫克（每周1毫克）7,12 - 二甲基苯并(a)蒽之前、期间和之后。观察到膳食LA水平与乳腺肿瘤发生率呈正相关，在前15周，8.4% LA日粮组的发生率最高，其次是4.5%组，然后是0.8% LA组。还注意到对潜伏期有明显的膳食影响，即分别在7,12 - 二甲基苯并(a)蒽停止给药后15周、12周和8周，0.8%、4.5%和8.4% LA日粮组出现40%的癌发生率。对所有肿瘤的组织病理学分析表明，主要类型是腺鳞癌，分别占含0.8%、4.5%和8.4% LA日粮的所有乳腺肿瘤的46.6%、54.1%和77.7%。第二常见的肿瘤是B型腺癌，在0.8%和4.5% LA日粮组中的发生率为33%，在8.4% LA日粮组中的发生率为22%。这些结果表明，SENCAR小鼠对7,12 - 二甲基苯并(a)蒽诱导的乳腺肿瘤发生具有较短的潜伏期，并且大鼠和小鼠的乳腺肿瘤发生以类似方式受到膳食LA的影响，尽管在SENCAR小鼠中膳食LA没有饱和效应。此外，高膳食LA被发现与腺鳞癌发生率增加特别相关，但与其他类型的乳腺肿瘤无关。
