A list of spontaneous renal tumors and of autonomous and partially autonomous derivatives of estrogen-induced renal carcinomas of Syrian hamsters is presented. More detailed descriptions of a new spontaneous renal carcinoma and of seven “autonomous” derivatives of estrogen-dependent renal carcinomas, all of which are available in a liquid nitrogen tumor bank, are included. Although androgen inhibits estrogen tumorigenesis in the Syrian hamster kidney, it can be substituted successfully for estrogen in maintaining growth of early transplant serial passages. In such transplants hormone dependency is usually lost between the 12th and 20th serial passages (autonomy). These autonomous derivatives of hormone-dependent renal tumors retain responsiveness to some steroidal hormones to varying extents. None of them has been as completely autonomous, i.e., hormone unresponsive, as the renal carcinoma of “spontaneous” origin. Although removal of hormonal support from early transplants of this tumor may inhibit or prevent tumor cell division, it does not necessarily prevent cell survival. A single transplant of one of these autonomous renal tumors may exhibit very marked histological differences during its life history. These differences reflect an action of the host upon the neoplasm and do not indicate progression. Hosts for autonomous renal tumors may show atrophic testes but relatively normal accessories, suggesting that the transplant may synthesize physiologically active sex steroids. Progression from hormone dependency to autonomy in serial passages of the estrogen-induced renal carcinoma occurs focally, resulting in cell areas with varying degrees of hormone dependency within single transplants and stressing the desirability of using cloned material for in vivo as well as in vitro transplantation studies. The demonstration of specific estrogen receptor proteins in the hamster kidney does not explain the relation of estrogen to tumor induction or the hormone responsiveness of the neoplasm. The roles of receptors, of stroma-epithelium relationships, of viral genomes, of immunogenicity, and antigenic differences in the induction of this tumor and in its progression from hormone dependency to autonomy are still not understood.


Much of the work reported here has received support from USPHS Research Grant CA-04516 from the National Cancer Institute.

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