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Lactation Induced by Luteotrophin in Women with Mammary Cancer. Growth of the Breast of the Human Male Following Estrogenic Treatment^*

( The Ben May Laboratory for Cancer Research, University of Chicago, Chicago 37, Ill.)

The breast of the human male can be induced to grow to a functionally mature state by the administration of estrogenic substances without additional exogenous steroid synergists. Spontaneous lactation was not observed in these men, but it was induced by luteotrophin.

The formation of milk in any amount by the breast is a criterion of functional maturity of the mammary epithelium. Luteotrophin induced the secretion of small amounts of milk in a group of women with mammary cancer and in a number of healthy women as well, and, in addition, in two human males to whom estrogenic substances had been administered for therapeutic purposes. Lactation did not occur in two normal males.

Many patients with carcinoma of the breast, even those in the 7th decade, secreted milk when the mammary gland was challenged with luteotrophin, despite the menopause and earlier removal of the ovaries; the primary mammary cancer in most of these women was adenocarcinoma. Other women with cancer of the breast failed to lactate when treated with luteotrophin; the primary neoplasm in most of these patients was undifferentiated.

A potential secretory capacity can be retained by the breasts of the human female in senility.

The prolonged administration of testosterone did not cause functional atrophy of mammary epithelium.

When lactation was induced in human beings, the secretion often persisted for many months; it lasted for 7 years in one man. In certain women with mammary cancer lactation ceased abruptly following the removal of the ovaries and adrenal glands, while in others it persisted. In three women with this persistent lactation, the secretion of milk was not stopped by the administration of diethylstilbestrol, testosterone, or progesterone.

^* This study was aided by grants from the Jane Coffin Childs Memorial Fund for Medical Research, the American Cancer Society on recommendation of the Committee on Growth of the National Research Council, and the Damon Runyon Memorial Fund for Cancer Research.

Received 12/ 3/53.