Influence of the Mammotropic Tumor MtTF4 on the Growth and Biochemistry of the R3230AC Mammary Carcinoma and Mammary Glands1

The effect of the mammotropic tumor, MtTF4, on the growth and biochemistry of the transplantable autonomous R3230AC mammary adenocarcinoma was investigated. The MtTF4 tumor, which secretes prolactin, growth hormone, and adrenocorticotropic hormone (ACTH) did not significantly alter the growth rate of the mammary tumor but did increase glucose-6-phosphate dehydrogenase (G6PD) activity in the R3230AC neoplasm when both tumors were implanted simultaneously in the same host. When implantation of the R3230AC mammary carcinoma was performed after the MtTF4 tumor had become established, the subsequent growth of the mammary tumor was reduced and the enzyme activities in the mammary neoplasm were decreased. This decreased rate of growth of the mammary neoplasm was due in part to the adrenal hyperactivity resulting from the ACTH secre tion of the mammotropic tumor, since both the growth inhibition and the decreased enzyme activities in the R3230AC carcinoma were partially reversed in the adrenalectomized tumor-bearing host. Estrogen treatment inhibited the rate of growth of the R3230AC neoplasm, in the presence or absence of the MtTF4 tumor, and this hormonal treatment induced increases in G6PD, malate dehydrogenase, and phosphoglucomutase activities in the mammary tumor. The dose of estradici valerate administered to these animals completely prevented further growth of the MtTF4 tumor. The response of the mammary glands of the tumorbearing hosts to the secretions of the MtTF4 tumor was reflected by elevations of the activities of all of the enzymes studied. These data are discussed in light of the projxjsed role of prolactin and mammary tumor growth.