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At least 955 records · Page 53Linked to original sources
PubMed1987

[Cellular immunity in prostatic cancer modified by Cytonal, Estrazyt and Turisteron].

The influence on the specific cell-mediated immunity (CMI) of the carcinoma of the prostate gland by the contra-sexual hormone therapy with Cytonal, Estrazyt and Turisteron is controlled. For this purpose the macrophage-electrophoresis-mobility test on the basis of allogenic tumour-associated antigen of the carcinoma of the prostate gland is used. As a result the use of Cytonal at least in the dosage hitherto used is no longer worth being advocated. Turisteron and Estrazyt, respectively, taking into consideration their pharmacokinetics and indication, prove to be immunologically optimal and without hesitation, respectively. Turisteron is the basic therapeutic in the androgen-dependent carcinoma of the prostate gland. Estrazyt should be reserved to primarily and secondarily hormone-refractory tumours. For the application of Estrazyt an additive immune stimulation seems to be worth taking into consideration.

Aged↗
PubMed1985

Endocrine therapy for prostate cancer.

Prostate cancer consists of epithelial and stromal elements that are heterogeneous with regard to androgen dependence. Nearly 80% of patients with symptomatic metastatic prostate cancer obtain prompt objective and subjective response to androgen deprivation. Surgical castration remains an effective form of therapy, has low morbidity, and obviates compliance problems with medical regimens. New LH-RH analogs offer complete medical androgen deprivation, appear as effective as estrogen therapy at 2-year follow-up, and have significantly lower cardiovascular side effects. Thus, LH-RH analogs may replace estrogen therapy for the medical management of metastatic prostate cancer. Androgen deprivation therapy has not been proved to prolong the survival of patients with prostate cancer. The optimal timing for initiation of endocrine therapy in these patients remains controversial. Techniques for predicting androgen dependence of prostate cancer are still evolving and are not yet applicable on a widespread clinical basis.

Adrenal Glands↗
PubMed1985

Management of metastatic prostatic cancer.

Current management techniques for metastatic prostatic cancer have given rise to controversies regarding the optimal timing, form, and degree of androgen deprivation. Low-dose diethylstilbestrol (DES) or orchiectomy decrease serum testosterone levels while posing less cardiovascular risk than high-dose DES. LH-RH analogues, such as leuprolide or buserelin, also inhibit testosterone production. Some studies suggest that some tumor cells may be relatively, rather than absolutely, androgen dependent. This has been the rationale for the combined use of a pure antiandrogen and an LH-RH agonist. Unfortunately, while this combination has been found effective in previously untreated patients, it has not been equally effective in those who have undergone prior therapy and demonstrated disease progression.

Adenocarcinoma↗
PubMed1985

[The effects of site-directed chemotherapy due to E2 as a drug carrier to the human endometrial adenocarcinoma cells in vitro].

The effects of Estracyt, a Nitrogen mustard (HN2) derivative of estradiol-17 beta versus the free HN2 on cell kinetics of the estrogen receptor positive human endometrial cancer cell line HEC-1 were investigated using flow cytometry. The results were as follows. The cell killing effects of Estracyt existed in a dependency on dose and time, whereas those of HN2 were dependent on dose alone. HN2 at 1 microgram/ml showed a marked increase in S phase and decrease in G0+1 phase. However, with equivalent doses of Estracyt at 10 micrograms/ml, even more remarkable was the accumulation in the G2+M phase. Synchronization at S phase with MTX showed no increase in sensitivity to these drugs on cells in S phase. Based on the above results, it was suggested that the free HN2 had an affect regardless of the cell cycle phase, whereas the effects of Estracyt corresponded to the cell cycle phase and Estracyt might have a fixed population of non-target cells existing in the G0+1 and S phase. Synchronization in the G1 phase with Sodium n-butylate could increase the target effects of Estracyt in S phase.

Adenocarcinoma↗
PubMed1975

Palliative treatment with oral Estracyte in disseminated prostatic carcinoma.

In Roswell Park Memorial Institute, between 1969 and 1974, a total of 32 patients with widespread metastasized carcinoma of the prostate were treated with oral Estracyt. Objectively demonstrable remissions were achieved in eight patients (8/32 equals 25%). Subjective improvement of their general condition was experienced by 15 patients (15/32 equals 47%). The toxicity of Estracyt manifests itself with gastrointestinal disorders, which in most cases are amenable to anti-emetic treatment.

Administration, Oral↗
PubMed1984

[Predictive value of the determination of receptors in carcinoma of the prostate].

The assay of hormone receptors in neoplastic tissues recognizes their sensitivity or autonomy with regard to the hormonal action. The hormone dependency of the activity of neoplastic tissues can be employed to select the cases having the highest probability to be benefited by the treatment with anti-hormones, castration or hypophysectomy, as in breast and prostatic cancers. Examining the case for prostatic cancer, the authors indicate that there is a good correlation between the predictive assay and the clinical evolution of the treated prostatic carcinoma employing the determination of cell receptors for 5-alpha-dihydrotestosterone (DHT) by exchange at 15 degrees C with the synthetic steroid methyltrienolone. The electrophoretic determination of binding of DHT to cell receptor a 4 degree C is a much less efficacious procedure.

Diethylstilbestrol↗