The administration of thyroxin at a dosage of 2.5 µg per 100 gm body weight daily for 7 months, beginning 10 days before methylcholanthrene treatment was started, only slightly altered the carcinogenic response of rats to methylcholanthrene. Chronic administration of propylthiouracil during the same period significantly inhibited mammary cancer induction by methylcholanthrene. However, in rats initially made hypothyroid by propylthiouracil administration, but in which the thyroidal status was subsequently reversed by administration of thyroxin (2.5 µg per 100 gm body weight daily) beginning 10 days after cessation of carcinogen feedings, the incidence and latency of appearance of mammary cancer were not different from control rats treated with methylcholanthrene only. These data suggest that modifications of the carcinogenic response of rats to methylcholanthrene as a result of altered thyroid hormone levels were due principally to the growth-promoting stimulus of thyroid hormone, or lack of it, upon established neoplastic cells.


This investigation was supported in part by Public Health Service Research Grant CA-05105 from the National Cancer Institute.

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