{"title":"Reproducibility of method and hormonal influences in induction of breast cancer in rats by gastric instillation of methylcholanthrene [abstract].","authors":"H Shay, M Gruenstein, C Harris","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>We have reported a high incidence and sex linkage of breast cancer in Wistar rats following gastric instillation of methylcholanthrene (J. Nat. Cancer Inst., 10:255, 1949, and 13:307, 1952). For this report, reproducibility of method and effects of estradiol and testosterone are evaluated in 103 male and 169 female rats which received methylcholanthrene 6 times a week throughout the experiments. The 169 female rats represent a pool of groups of 10 or more animals used as controls for experiments run during the past several years. Tumor incidence ranged from 73-100%, with a combined average of incidence 82%. The high incidence of pituitary tumors in both sexes treated with estradiol; the decrease in breast cancers in methylcholanthrene-treated females receiving testosterone or estradiol; and the incidence of breast cancers in both sexes receiving only estradiol permit speculation regarding the role of the pituitary gland in induction of breast cancer by methylcholanthrene in our experiments. The sharp drop in incidence of breast tumor in animals receiving methylcholanthrene and estradiol suggests involvement of a pituitary factor or factors in induction of breast tumors by methylcholanthrene; with the development of pituitary tumors in animals receiving estradiol, these factors may no longer be available. Estradiol-induced breast cancer in the rat may utilize a mechanism independent of the pituitary.</p>","PeriodicalId":85350,"journal":{"name":"Proceedings of the American Association for Cancer Research","volume":"2 2","pages":"146"},"PeriodicalIF":0.0,"publicationDate":"1956-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"22010143","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"The effect of hypophysectomy on 9,10-dimethyl-1,2-benzanthracene-induced carcinogenesis [abstract].","authors":"R L Noble, J H Walters","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>In view of the findings of Moon, Simpson, and Evans (Science, 116:331,1952) that the hypophysectomized rat was refractory to the carcinogenic effect of methyl-cholanthrene, similar experiments have been conducted but using the more powerful carcinogen 9,10-dimethyl-1,2-benzanthracene. The results of 2 separate experiments were as follows: All animals received 5 mg in sesame oil of the carcinogen intramuscularly. In the control animals, 15 showed discrete sarcoma out of 21 animals in 4-5 months. In the hypophysectomized animals only 3 showed comparable sarcoma, but in 7 there was marked abnormal proliferation of fibroblasts suggestive of malignant change. 9 animals were negative, although serial sections were not made. In addition to these findings it was noted that in control animals 6 mammary tumors developed in tissue adjacent to the injection site. 4 of these were of a malignant nature. In the hypophysectomized group no mammary changes were observed. Although these findings are somewhat in accord with the original observations it is believed that the change is quantitative rather than qualitative. Unfortunately, the hypophysectomized animals survived only 3-4 months, and the findings are suggestive that the malignant process occurs but more slowly in the absence of the normal pituitary function. The changes in mammary tissue would seem more clearcut, but are being repeated on a larger series of animals.</p>","PeriodicalId":85350,"journal":{"name":"Proceedings of the American Association for Cancer Research","volume":"1 2","pages":"35-6"},"PeriodicalIF":0.0,"publicationDate":"1954-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"22034256","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"The co-action of estrogen in the induction of tumors of the mouse uterus treated with 20-methylcholanthrene [abstract].","authors":"B V Hall, Balder Rb, K Hamilton","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Over 200 young mature and mature CF1 mice were ovariectomized and their uterine horns implanted bilaterally with circa 2 mg methylcholanthrene (MCA) by trocar. Subcutaneous injections of 20 mcg diethylstilbestrol in 0.05 ml oil were then made 3x weekly in equivalent groups for 0, 4, 6, 10, 12, 14, 16, 18, and 20 weeks. All animals died or were sacrificed by 180 days following MCA implantation. Nearly 1/2 of the 57 mice surviving estrogen treatment and living at least 100 days after MCA implantation developed uterine tumors. Most of the affected mice developed tumors in both cornua. Tumors in mice receiving estrogen for the longer periods were especially large and aggressive. Histologically, they were predominantly sarcomatous, but adenocarcinomas were induced in the approximate ratio of 1:4. The incidence of tumors in mice treated with estrogens for 12-20 weeks was significantly higher than in those given extrogen 4-10 weeks. Only 1 prominent uterine tumor was found in 8 mice which survived 102-168 days after bilateral MCA implantation and 12 subcutaneous injections of 60 mcg diethylstilbestrol in 4 weeks. Diethylstilbestrol, when administered for a sufficient period, seemingly acts as a cocarcinogen in mice, accelerating the induction of uterine tumors by MCA and perhaps stimulating their growth.</p>","PeriodicalId":85350,"journal":{"name":"Proceedings of the American Association for Cancer Research","volume":"1 1","pages":"23"},"PeriodicalIF":0.0,"publicationDate":"1953-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"22025156","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}