Treatment of prostatic cancer with LH‐RH analogues

Abstract

Twenty-one of 32 patients with locally advanced prostatic cancer (stage C) were treated with the LH-RH analogue Buserelin for 7-19 months. After an initial sequence of subcutaneous injections, treatment was continued with intranasal spray application (three daily doses of 400 micrograms each) which ensured maintenance of serum testosterone within the range seen in castrated men. To evaluate the response of the primary tumor to Buserelin, cytological regression was established for all patients by fine-needle aspiration biopsy every 3 months. The cytological results corresponded with those of DNA analyses of single-cell cytophotometry showing a statistically significant drop of the grade of aneuploidy or polyploidy when the prostatic carcinoma responded positively to Buserelin therapy. Seventeen of 21 patients treated with the potent LH-RH analogue showed good therapy response. Four patients with no cytological signs of tumor regression received secondary treatment with estramustine phosphate because of hormone resistence. One patient had to be crossed over to cyclophosphamide, the third drug, for clinical progression after 15 months. Essential side effects have not been observed. Continuous treatment of locally advanced prostatic cancer with Buserelin, combined with close control of the patient, offers not only a real alternative to surgical castration--as the patient is spared the psychical stress of orchiectomy--but also to estrogen therapy with its risk of cardiovascular side effects.

Nuclear DNA Analysis: The Relevance of Ploidy, DNA Heterogeneity and Phases of the Cell Cycle in 329 Patients with Prostatic Carcinoma

“…The DNA heterogeneity of tumor cell nuclei in malignant tumors of different organs has become very important clinically during the last few years because of its relation to tumor behavior before and during therapy [1,2,4,6,9,12,15,19,23].…”

Investigation of the Combination of the Agonist D-Trp-6-LH-RH and the Antiandrogen Flutamide in the Treatment of Dunning R-3327H Prostate Cancer Model

“…A novel approach to endocrine therapy for prostatic cancer is based on the use of superactive agonists of LH-RH [ 12,[23][24][25][26][27][28][29][30][31][32][33][34][35][36]38461. Chronic administration of these analogues leads to pituitary desensitization, down-regulation of receptors, and inhibition of pituitary-gonadal axis manifested by a marked decrease in the secretion of LH, FSH, and sex steroids.…”

Effect of LHRH analog on the seminal vesicles evaluated by transrectal sonography

“…On the other hand, LHRH analog is now widely employed for the treatment of prostatic cancer as "medical castration" [2]. Soon after medication, the serum T level increases transiently compared with the baseline level for a few days and decreases rapidly subsequently.…”

“…First, the MHA of the seminal vesicles decreased finally in all cases. The cause of the decrease of MHA was explained from the following evidence: (1) in the animal experiments, the gland and stroma of the seminal vesicles changed by atrophy with a depletion of T after LHRH analog treatment; the decrease in the weight of the seminal vesicles mainly depended on the dose administered [8]; (2) protein synthesis in the seminal vesicles was dependent on circulating T [9]; and ( 3 ) T changed the transmitter content of the adrenergic nerves and the contractivity of the seminal vesicles [lo].…”

“…A depletion of endogenous androgen induced by castration leads easily to their atrophy and a repletion restores them in rats [ 11. Recently, LHRH analog is used for the treatment of patients with prostatic cancer as "medical castration" [2]. The Serum testosterone (T) level in such patients shows a rapid increase beyond the baseline, and a subsequent decrease to the castration level.…”