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Characterization of Steroid Hormone Receptors in the Dunning R-3327 Rat Prostatic Adenocarcinoma¹

Department of Biochemistry and Cancer Research Institute [F. S. M.], University of Southern California School of Medicine, and Department of Urology [R. T. C., M. D. C.] and Pathology [E. B. H.], Los Angeles County-University of Southern California Medical Center, Los Angeles, California 90033

We have characterized several histological variations of the transplantable R-3327 prostatic adenocarcinoma and correlated these histological types with steroid hormone receptor content. One type is clearly an adenocarcinoma. This tumor is hormonally responsive (grows better in male than in female rats) and contains substantial amounts of both androgen and estrogen receptors. In contrast another histological type, a fibrosarcoma developed in passages of the R-3327 tumor grows rapidly in female and in intact and castrated male rats. This histological type does not contain either the androgen or estrogen receptor as determined by sucrose density gradient centrifugation. There is also a third histological variant that is classified as a carcinosarcoma. These tumors contain histological elements of both adenocarcinoma and fibrosarcoma and are also hormonally responsive; they contain lower receptor levels than do the adenocarcinomas but more than the fibrosarcomas.

The androgen receptor found in the different histological forms of the tumors has a sedimentation coefficient of 7.8S, and the dissociation constant for methyltrienolone is about 4 x 10^-9 M. The estrogen receptor has a sedimentation coefficient of 8.3S, and the dissociation constant for estradiol is about 4 x 10^-10 M.

Plasma of the Copenhagen rat was shown to be devoid of androgen or estrogen receptors, and the normal prostate of Copenhagen rats was shown to contain low levels of an androgen receptor but no estrogen receptor.

¹ Supported in part by USPHS National Cancer Institute Grant CA 14089 to the LAC/USC Cancer Center, by USPHS National Cancer Institute Grant CA 21746, and by American Cancer Society Institutional Research Grant IN-21-P to the University of Southern California.

² To whom requests for reprints should be addressed.

Received 12/19/77. Accepted 5/19/78.