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( Department of Experimental Biology, The Weizmann Institute of Science, Rehovoth, Israel)
Untreated LAF1 mice used in the present series (which are generally considered to be free of the mammary tumor agent) did not develop mammary adenocarcinomas spontaneously. Treatment with methylcholanthrene also failed to produce mammary tumors in this strain in the absence of hormonal stimulation of the mammary tissue (though it did produce leukemia and squamous carcinomas). Continuous stimulation of the mammary gland by the mammotrophic stimulating hormone produced mammary tumors in about 9 per cent of mice, with lung metastases in some cases. Methylcholanthrene, when applied on nonstimulated normal breast tissue, followed by mammotrophic hormone stimulation as a possible promoter, did not increase the percentage of mammary tumors above the control level. Methylcholanthrene did increase the mammary tumor incidence to 35 per cent in the case when the mammary glands were previously stimulated by mammotrophin hormone for 5 weeks, with simultaneous action of methylcholanthrene plus the mammotrophin hormone for 1 subsequent weeks. Mammary gland stimulation for 6 months, followed by methylcholanthrene paintings alone, elicited only a moderate increase in mammary tumor incidence (16.6 per cent). Whether the function of mammotrophin in mice is mainly to induce hyperplastic nodules, necessary as a primary stage of mammary tumor development, or whether it serves also as a promoting agent in mammary tumor development, requires further elaboration. The mammotrophic pituitary tumor used in these experiments, as a natural source of mammotrophin, exhibited somatotrophic activity and also a possible luteotrophic action.
* This work was supported in part by Grant DRG 493A from the Damon Runyon Memorial Fund for Cancer Research.
Received 1/26/61.
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