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Query: UMLS:C0007112 (
prostatic adenocarcinoma
)
2,574
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Prostate cancer has an unpredictable natural history if left untreated, particularly if the neoplasm is discovered when it is apparently organ confined. To our knowledge we report the first case of organ confined
adenocarcinoma of the prostate
in a cardiac transplant recipient. The therapeutic decision is complicated by the uncertainty of the impact of continued immunosuppression on
tumor growth
. Although the effect of immunosuppression on the growth of prostate cancer is unknown, our patient was treated within the accepted guidelines for similarly affected nonimmunosuppressed individuals. Improvements in long-term survival rates of patients undergoing cardiac transplantation warranted radical surgical ablation as treatment for this man with clinically organ confined prostate cancer.
...
PMID:Prostate cancer after heart transplantation. 796 56
Male Copenhagen x Fisher F1 rats, transplanted with the androgen-sensitive Dunning R3327 PAP rat
prostatic adenocarcinoma
, were castrated when tumor volumes were approximately 1300 mm3. The rats were thereafter followed with measurements of tumor volume. Castration stopped
tumor growth
, but some of the tumors started to regrow after 7-36 weeks. These tumors relapsing from castration treatment were now considered to be androgen-insensitive. In this study, we defined relapse as the time when the tumor volume had increased to 200% of the volume at the time for castration. At this time, the rats were treated either with estradiol-17 beta (E2, 50 micrograms s.c. daily) or vehicle for 8 weeks. After this period, tumor morphology was examined. The tumors in the vehicle-treated group were heterogeneous, and both highly and more dedifferentiated parts were present. The
tumor growth
rate was correlated to the epithelial cell nuclear size and its variance, and to the mitotic index. In the E2-treated group,
tumor growth
rate was retarded throughout the treatment period, and dedifferentiated tumor areas were rare. Estrogen treatment resulted in a reduction of nuclear area and mitotic index, a changed nuclear shape, and an increased apoptotic index compared to that in vehicle-treated tumors. By castration, it is possible to induce an alteration of the androgen-sensitive Dunning R3327 PAP tumor phenotype to an androgen-insensitive tumor with an altered morphology. Estradiol-17 beta apparently inhibits not only the growth, but also postpones the castration-induced dedifferentiation of the tumor.
...
PMID:Estrogen treatment postpones the castration-induced dedifferentiation of Dunning R3327-PAP prostatic adenocarcinoma. 802 7
Hyperthermia alone or with radiation is used therapeutically for localized solid tumors. Clinical experience shows that sustained tumor temperature exceeding 45 degrees C damages normal tissue. Any agent that enhances the effects of hyperthermia at or below this temperature may have clinical relevance. Lonidamine and hyperthermia were tested on the Dunning R3327G rat
prostatic adenocarcinoma
. Using colony-formation assays, cytotoxic effects of each agent alone and in combination were quantified. Lonidamine to 100 micrograms/ml was not significantly toxic, but in combination, it enhanced cytotoxicity. Survival patterns after fractionated hyperthermia revealed a rapid development and decay of thermotolerance. Measurement of cell-cycle progression following a single dose of hyperthermia revealed a reduction of S-phase cells, and subsequent accumulation in G1 over 24 hours. Combination treatment of tumor-bearing rats significantly reduced
tumor growth
rate when compared with individual agents. These results suggest a potential use of lonidamine in hyperthermic therapy of prostate tumors.
...
PMID:Enhancement of hyperthermic toxicity by lonidamine in the Dunning R3327G rat prostatic adenocarcinoma. 811 78
The present study was designed to determine if estramustine phosphate (EMP) could potentiate the effects of irradiation on the Dunning (R3327)
prostatic adenocarcinoma
in rats. Two groups of male Copenhagen x Fisher F1 rats carrying bilateral tumors in the flank were used. Irradiation was given with a linear accelerator 6 MV, in a dose of 6 Gy/day for 4 days to the tumor on one side while the tumor on the other side served as control. EMP (360 micrograms/24 hours) was administered with osmotic pumps to one group of rats for 2 weeks, starting 1 week before irradiation. Tumor growth was calculated by measuring tumor volume, and tumor blood flow was measured 8 weeks after treatment. Irradiation alone effectively delayed
tumor growth
and EMP enhanced these effects. Tumor blood flow was stimulated by EMP treatment irrespective of radiotherapy. Volume density of tumor epithelium was effectively decreased by irradiation but no significant effects could be seen after EMP. In conclusion, the present study shows that EMP potentiates irradiation on rat
prostatic adenocarcinoma
, and further evaluation of this therapeutic approach in the clinical treatment of prostatic carcinoma is thus justified.
...
PMID:Estramustine potentiates the effects of irradiation on the Dunning (R3327) rat prostatic adenocarcinoma. 830 47
Prostatic inhibin (PI) is a M(r) 10,700 protein found in human seminal plasma and is secreted by the prostate. Recognition of alteration of PI levels in prostatic diseases prompted us to investigate its effect on an animal
prostatic adenocarcinoma
model, the Dunning R3327G rat tumor. PI not only inhibited in vitro growth of tumor cells but also suppressed
tumor growth
in vivo. A dose-dependent inhibition of both the clonogenic cell growth and rate of proliferation (DNA synthesis) was observed in tumor cell cultures incubated with purified PI. These inhibitory activities were similar in both androgen-dependent and androgen-independent Dunning tumor cell lines. A functional decapeptide of PI was also found to inhibit Dunning tumor cell colonies in a dose-dependent manner. Daily injection of purified PI into tumor-bearing rats suppressed the
tumor growth
. A 58% reduction in tumor weight and a 2-fold reduction in
tumor growth
rate were observed over a 15-day treatment period. Continued treatment with PI significantly suppressed the
tumor growth
rate by nearly 3-fold. These findings clearly demonstrate a potential application of PI for treating human
prostatic adenocarcinoma
.
...
PMID:Human prostatic inhibin suppresses tumor growth and inhibits clonogenic cell survival of a model prostatic adenocarcinoma, the Dunning R3327G rat tumor. 840 73
Metastasis represents a hallmark of the tumor cell's escape from normal cellular behavior to acquired invasive and migratory style. Metastasis of prostate cancer (Pca) depends upon the interplay of a series of hematogenous and hematopoietic factors. We investigated the role of some of those factors implicated in the dissemination process in two separate sublines of
adenocarcinoma of the prostate
. Our data revealed that (1) the urokinase plasminogen activator activity was significantly higher in R3327-AT3, an aggressive metastatic tumor, as compared to R3327-G, a nonmetastatic tumor of the prostate, (2) the concentration of platelets decreased, and the platelet-aggregating activity increased significantly when the platelets were reacted with exogenous aggregating agents and tumor effusions to suggest that activation of the hemostatic system could protect tumor cells from immunosurveillance and facilitate the process of hematogenous dissemination, and (3) transferrin, which has been reported to have a growth-promoting effect on Pca, did not show any appreciable effect on
tumor growth
but did alter the level of in vitro adherence which possibly could lead to better attachment and increased invasive behavior of tumor cells.
...
PMID:Metastatic behavior of prostatic tumor as influenced by the hematopoietic and hematogenous factors. 898 19
The hypothesis that
tumor growth
is angiogenesis dependent has been documented by a considerable body of direct and indirect experimental data. A prerequisite for the development of novel anti-angiogenic agents is the design of drugs that would be active only on those endothelial cells with an angiogenic phenotype. We took advantage of the anti-idiotypic strategy to obtain circulating agonists specific for the vascular endothelial growth factor receptor KDR/flk-1 (J-IgG). They induced in the absence of VEGF cell proliferation in vitro and angiogenesis in the corneal pocket assay either through local or systemic delivery. Intraperitoneal injections of J-IgG in nude mice grafted with a
prostatic adenocarcinoma
led to tumor enlargement associated with an increase in both tumor vascularization and proliferation. In contrast KDR/flk-1 overstimulation had no detectable effect on normal tissues. These data underline that KDR/flk-1 is a functional marker of the angiogenic phenotype of endothelial cells.
...
PMID:Systemic activation of the vascular endothelial growth factor receptor KDR/flk-1 selectively triggers endothelial cells with an angiogenic phenotype. 935 46
Combined androgen blockade using a pure antiandrogen in association with a LHRH agonist or surgical castration is the most logical approach. This paper demonstrated that flutamide combined with leuprorelin acetate produced a significant reduction in the growth rate of Dunning R3327-H
prostatic adenocarcinoma
. Dunning R3327-H
prostatic adenocarcinoma
, provided by Dr. Norman H. Altmann (University of Miami, USA) was subcutaneously inoculated into the lateral region of male Copenhagen x Fischer F1 hybrid rat abdomen. The efficacy of the
tumor growth
rate was evaluated by measuring tumor size at 10 weeks after the inoculation. Flutamide was orally administered for 10 weeks and leuprorelin acetate was subcutaneously administered every 4 weeks. The effective dose of flutamide and leuprorelin acetate was determined in preliminary studies, and the following doses were used in the study; 15 mg/kg for flutamide, 0.1 mg/kg or 0.4 mg/kg for leuprorelin acetate. In combination of flutamide with leuprorelin acetate at 0.1 mg/kg and 0.4 mg/kg, the tumor inhibition was 94% and 97%, respectively. In addition, the weight of accessory sex organs coincided with the antitumor effect. Taking the above results into consideration, combined androgen blockade using flutamide and leuprorelin acetate may have some beneficial effect on prostatic cancer.
...
PMID:[Combination effect of flutamide and leuprorelin acetate on growth of Dunning R3327-H prostatic adenocarcinoma in rats]. 953 Mar 63
The purpose of this study was to determine the effectiveness and toxicity of local continuous immunotherapy of prostatic cancer. A group of 60 young male Copenhagen rats with Dunning
adenocarcinoma of the prostate
, implanted subcutaneously into both flanks, after proven
tumor growth
, were treated with either human interleukin-2 (IL-2) depot preparations (n = 30) or albumin (placebo) depot preparations (n = 30) implanted directly into one tumor site. IL-2 depots released IL-2 reliably for more than 24 days. The rat serum was tested during treatment for human IL-2, possibly absorbed from depots, and for rat interferon gamma. IL-2 treatment reduced
tumor growth
significantly (P < 0.001) compared with albumin-treated sites or untreated contralateral sites. No toxicity was observed during treatment. Neither human IL-2 nor rat interferon gamma was detected in the serum, which indicates an exclusively local IL-2 effect. IL-2 depot preparations reduce
tumor growth
in Dunning
adenocarcinoma of the prostate
significantly without toxicity.
...
PMID:Intratumoral depot interleukin-2 therapy inhibits tumor growth in Dunning adenocarcinoma of the prostate implanted subcutaneously in rats. 962 Feb 19
Angiogenesis is thought to play critical roles in local
tumor growth
and eventual metastasis. No studies have examined the expression of platelet-derived endothelial cell growth factor (PD-ECGF) in prostatic tissues. Prostatic tissues were obtained from 36
prostatic adenocarcinoma
patients. We assessed the expression of PD-ECGF using ELISA and immunohistochemistry. The mean level of PD-ECGF in prostatic adenocarcinomas was higher than that in neighboring normal prostatic tissues in ELISA. Immunohistochemistry showed that the expressions of PD-ECGF, which were associated with increase of microvessel count, were found in the endothelial cells, macrophages, lymphocytes, or fibroblasts. These results suggest that PD-ECGF is involved in the development of
prostatic adenocarcinoma
.
...
PMID:Expression of platelet-derived endothelial cell growth factor in prostatic adenocarcinoma. 1020 84
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