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Characterization of a Transplantable Lactating Mammary Tumor: Endocrinological, Morphological, and Biochemical Aspects^*

( Squibb Institute for Medical Research, New Brunswick, N. J.)

A transplantable mammary tumor of the Fischer rat, the R3230AB, lactates in response to estrogen treatment. This autonomous-responsive tumor was inhibited by either estrogen or androgen treatment in both intact and castrated hosts. Hydrocortisone and progesterone inhibited tumor growth only at high dose levels. Lactation was induced by estrogen treatment and appeared to be slightly enhanced when prolactin was administered in combination with the estrogens. Lactation was always accompanied by inhibition of tumor growth. This lactational response could be obtained following thawing of frozen tumor tissue. Secretory activity has been maintained for 18 months of continuous hormone treatment.

Characteristic morphological changes of the tumor resulted from hormone treatments. Estrogen treatment, either alone or in combination with prolactin, produced extensive secretory activity in the epithelial cell elements of the tumor, whereas treatment with androgen depressed the epithelial cells and appeared to stimulate the stromal elements. Biochemical studies showed that two- to threefold increases in glucose-6-phosphate dehydrogenase and TPN-malic enzyme activities accompanied induction of the lactational state by estrogens. Androgens caused a decrease in TPN-malic enzyme activity. In vitro utilization of glucose or malic acid substrates was 2–3 x higher in the lactating tumor. RNA/DNA ratios were only slightly increased by estrogen treatment and were not affected by the other hormone treatments investigated. This transplantable tumor has retained its hormone responsiveness and appears to represent a tumor in which weight, morphology, and biochemical characteristics can be correlated.

^* Work done under Contract No. Sa-43-ph-2395 from the Cancer Chemotherapy National Service Center, National Cancer Institute, National Institutes of Health.

Presented in part at the 54th Annual Meeting of the American Association for Cancer Research in Toronto, Canada, May 23–25, 1963. An abstract appears in Proc. Am. Assoc. Cancer Res., 4:28, 1963.

Received 12/ 5/63.