Effect of estrogen and antiestrogen therapy in rats bearing mesenchymal tumors.

We applied both hormonal and antiestrogen treatment in female Wistar rats to analyze the estrogen dependence of the growth of sarcomas induced with 9,10-dimethyl-1,2-benzanthracene. Animals bearing tumors of 10 mm in diameter were divided at random into five groups and submitted to different treatments during 24 weeks. The treatment with ovariectomy and tamoxifen in tumor-bearing animals resulted in tumor growth suppression and prolonged survival by a protection against the lethal tumor. On the other hand, the estrogen treatment exerted an adverse effect showing a faster growth of the tumors and a great decrease in survival. In summary, the antiestrogen treatment can have an antitumor effect in mesenchymal tumors, possibly by modifying the immunological status of the host.

Relationship between immune state and tumor growth rate in rats bearing progressive and non-progressive mammary tumors.

Impaired immune responses occur frequently in cancer patients or in tumor-bearing animals, but the mechanisms of the tumor-induced immune defects remain poorly understood. The aim of the present study was to determine the relevance of the immune system in the control of tumor growth. We have developed a model of progressive and non-progressive mammary tumor, chemically induced in female Wistar rats. In this model we evaluated the development of an immune response after immunization of rats bearing progressive and non-progressive tumors with a non-related antigen, such as sheep red blood cells. We also studied the activation state of peritoneal macrophages from animals bearing tumors by evaluating the production of free radicals. Our findings indicated that the cell-mediated immunity in rats bearing progressive tumors fails to respond to heterologous antigen in vivo, as demonstrated by a negative delayed-type hypersensitivity reaction, and is accompanied by minor nitric oxide production by peritoneal exudate cells as well as a lower capacity for macrophage activation. The study of non-progressive tumor-bearing rats indicated that the cell-mediated immune response was intact and an activated state of macrophages was found in vivo. The results described in this paper should be taken into account when therapies based on cancer vaccines are chosen for the treatment of cancer.

Time-course study of cellular immune response and testosterone metabolism in an autoimmune model for chronic prostatic inflammation.

PURPOSE: Little is known of the etiology and pathogenesis of chronic inflammatory prostate diseases of noninfectious origin. In our experimental autoimmune rat model for chronic prostatic inflammation (CPI) we evaluated, in a time-course study, the specific cellular immune response to male accessory glands (MAG) and metabolic activity in the prostate gland. Results obtained in CPI rats were compared with data from rats immunized with kidney homogenate as well as from non-treated rats. MATERIALS AND METHODS: Specific cellular immune response against MAG antigen(s) was studied by delayed type hypersensitivity (DTH) and lymphocyte proliferation tests. The prostate 5alpha-reductase activity was studied in prostate homogenates by thin layer chromatography (TLC). RESULTS: DTH values were positive in MAG treated rats sacrificed at days 7 and 28 after first immunization (FI) (p < or = 0.05) in relation to kidney treated and non-treated rats. When we analyzed the proliferative responses to MAG antigen(s), an antigen specific proliferation, as shown by the mean [3H]thymidine uptake (cpm), was observed in rats sacrificed on days 14 and 28 (p < or = 0.05) after FI. The metabolic studies indicated that the 5alpha-reductase activity decreased slightly in MAG treated groups at day 14 after FI and diminished significantly at the end of CPI development. CONCLUSION: These data reveal that the prostatic endocrine cell destruction during CPI could be a consequence of immune/inflammatory cell mediated processes.