Spontaneous and estrogen-produced tumors in Nb rats and their behavior after transplantation.
Tumors in rats of the Nb strain, arising either spontaneously or after prolonged treatment with s.c. pellets of estrogen, were transplanted to establish whether hormone conditioning was required for their growth. Whereas all spontaneous tumors arising in males and many of those in females were autonomous on transplant, most of those arising in estrogenized rats continued to require hormones for growth after transplantation. The latter included carcinomas of the adrenal cortex, breast, pituitary ectopic tissue, ovary (thecomas), Leydig cells of testis, thymus, pancreas,salivary glands, oribital gland (fibroadenoma), liposarcoma, and lymphoma. Many of the tissues of origin of the tumors have not been considered to be under theinfluence of estrogens. A type of hormone-responsive tumor that was inhibited by estrogen and that grew only in normal rats is described. Ali estrogens tested, including estriol , were interchangeable in action. The incidence of the more common tumors of the adrenal, breast, and pituitary was very low in normal rats, but higher in females. All tumors were more common after estrogenization in both sexes, particularyly in older animals. The secretion of steroids and pitiutary hormones by many tumors led to obvious biological effects. Pituitary secretion led to severe lesions frequently associated with diseases in humans, but the signs of such diseases in the rat apparently were hormone dependent and disappeared if the tumor was removed. The overall results raised the possiblity that estrogens were not carcinogenic per se but stimulated the growth of previously altered cells and that, following their transplantation, this hormone requirement was retained. Irrespective of the mechanism of carcinogenesis, hormone-dependent tumor growth was not irreversible but was controlled in an unexpectedly wide spectrum of organs by exogenous estrogen. Host factors may play a major role in controlling the growth of many tumors and the ultimate course of the disease.
D000306:Adrenal Cortex Neoplasms / Q000139:chemically induced; D000818:Animals; D002273:Carcinogens; D002828:Choristoma / Q000139:chemically induced; D004967:Estrogens / Q000494:pharmacology / Q000633:toxicity*; D005260:Female; D007680:Kidney Neoplasms / Q000139:chemically induced; D008223:Lymphoma / Q000139:chemically induced; D008297:Male; D008325:Mammary Neoplasms, Experimental / Q000139:chemically induced; D008954:Models, Biological; D009368:Neoplasm Transplantation; D009374:Neoplasms, Experimental / Q000139:chemically induced*; D009918:Orbital Neoplasms / Q000139:chemically induced; D010051:Ovarian Neoplasms / Q000139:chemically induced; D010190:Pancreatic Neoplasms / Q000139:chemically induced; D010911:Pituitary Neoplasms / Q000139:chemically induced; D051381:Rats; D012468:Salivary Gland Neoplasms / Q000139:chemically induced; D012737:Sex Factors; D013736:Testicular Neoplasms / Q000139:chemically induced; D013953:Thymus Neoplasms / Q000139:chemically induced; D002583:Uterine Cervical Neoplasms / Q000139:chemically induced; D014594:Uterine Neoplasms / Q000139:chemically induced; D014625:Vaginal Neoplasms / Q000139:chemically induced
D002273:Carcinogens; D004967:Estrogens