trelstar has been researched along with Liver-Neoplasms* in 6 studies
1 review(s) available for trelstar and Liver-Neoplasms
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Hepatocellular carcinoma during hormonotherapy for prostatic cancer.
A case is reported of a poorly differentiated hepatocellular carcinoma that occurred in a 65-year-old patient who was on hormonotherapy for prostatic adenocarcinoma. The diagnosis of hepatocellular carcinoma was made 3 months after the initiation of a hormonal treatment with cyproterone acetate (for 1 month) and an LH-RH agonist. A cause and effect relationship between steroid hormones and hepatocellular carcinoma has been advocated in the literature. The occurrence of hepatic malignancy after a short hormonal therapy makes our case very unusual. Topics: Adenocarcinoma; Aged; Antineoplastic Combined Chemotherapy Protocols; Carcinoma, Hepatocellular; Cyproterone Acetate; Humans; Liver Neoplasms; Male; Neoplasms, Second Primary; Prostatic Neoplasms; Triptorelin Pamoate | 1994 |
2 trial(s) available for trelstar and Liver-Neoplasms
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Evaluation of antiandrogen therapy in unresectable hepatocellular carcinoma: results of a European Organization for Research and Treatment of Cancer multicentric double-blind trial.
The aim of the study was to evaluate the efficacy of antiandrogen therapy on overall survival and response in unresectable hepatocellular carcinoma (HCC).. A total of 244 patients with unresectable HCC were included in this multicentric double-blind trial. According to a two-by-two factorial design, patients were randomly assigned to receive one of the following treatments: pure antiandrogen plus placebo (A+P group, 60 patients); luteinizing hormone-releasing hormone (LHRH) agonist plus placebo (LHRH+P group, 62 patients); pure antiandrogen plus LHRH agonist (A+LHRH group, 62 patients); or placebo plus placebo (P+P group, 60 patients). Pure antiandrogen consisted of Anandron (Roussel-Uclaf Laboratory, Romainville, France) administered orally (300 mg daily for 1 month, then 150 mg daily). LHRH consisted of goseriline acetate (3.6 mg) or triptoreline (3.75 mg) administered monthly by subcutaneous injection. Treatment was given until death. Response was evaluated every 8 weeks according to World Health Organization (WHO) criteria.. Six patients were considered ineligible. One patient had a complete response (A+P arm) and three had a partial response (two in the LHRH+P arm and one in the A+LHRH arm). An overall log-rank test did not demonstrate any significant difference in survival among the four arms. Taking the factorial design into account, comparison of survival showed no significant difference between Anandron-containing regimens and others, or between LHRH-containing regimens and others. No serious side effects occurred for any regimen.. This controlled study shows clearly the lack of efficacy of androgen treatment in unresectable HCC. Topics: Androgen Antagonists; Antineoplastic Agents; Antineoplastic Combined Chemotherapy Protocols; Carcinoma, Hepatocellular; Double-Blind Method; Female; Gonadotropin-Releasing Hormone; Goserelin; Humans; Imidazoles; Imidazolidines; Liver Neoplasms; Male; Survival Rate; Triptorelin Pamoate | 1998 |
Treatment of hepatocellular carcinoma with combined suppression and inhibition of sex hormones: a randomized, controlled trial.
We tested the hypothesis that a combination of sex hormone suppression and inhibition of their target receptors might improve survival for patients with hepatocellular carcinoma (HCC). Eighty-five consequent, previously untreated HCC patients with inoperable disease, were randomized to receive the luteinizing hormone-releasing hormone (LR-RH)-analogue triptorelin and the antiestrogen tamoxifen (33 patients) or triptorelin plus the antiandrogen flutamide (23 patients), or only placebo (29 patients) in a double blind fashion. All groups were comparable as to age, sex, tumor extension, underlying cirrhosis and biochemical parameters. The tamoxifen (TMX) group had a significantly longer survival (282 days) compared with flutamide (112 days) and with placebo (127 days) groups (P = .0238, log rank test). The upper quartile of patients in the TMX group lived 384 days or longer, and most of them (57.1%) were women (P < .0005), in contrast to the upper quartile of the placebo (170 days, 16.7% women) and the flutamide group (134 days, 33.3% women). The calculated tumor volume doubling time (TVDT) was significantly higher in the TMX group (296 days) than in the other two groups (99 and 101 days for placebo and flutamide groups, respectively, P = .023). In a Cox proportional hazards model, the TMX treatment, along with the baseline Okuda's HCC stage, the hepatitis B surface antigen, the portal vein diameter, the carcino embryonic antigen (CEA) and a self-assessment score of quality of life, were covariates predicting survival. Although the degree of serum sex hormone suppression was not a significant predictor of survival, the interaction of female sex and TMX treatment, it was (P = .0052).(ABSTRACT TRUNCATED AT 250 WORDS) Topics: Analysis of Variance; Androgens; Carcinoma, Hepatocellular; Double-Blind Method; Drug Therapy, Combination; Estradiol; Estrone; Female; Flutamide; Follicle Stimulating Hormone; Follow-Up Studies; Humans; Liver Neoplasms; Luteinizing Hormone; Male; Middle Aged; Neoplasm Staging; Placebos; Probability; Survival Rate; Tamoxifen; Time Factors; Triptorelin Pamoate | 1995 |
3 other study(ies) available for trelstar and Liver-Neoplasms
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Metastatic primary seminal vesicle adenocarcinoma: management of a rare tumour with multiagent chemotherapy and hormonal therapy.
Primary seminal vesicle adenocarcinoma is one of the rarest genitourinary cancers. The pathogenesis is unknown and clinical manifestations are protean. There is no defined treatment for this disease and various combinations of surgery, chemotherapy, radiation therapy and hormonal therapy have been used in the past. Here, we have reported a primary seminal vesicle adenocarcinoma with hepatic metastases, managed with multiagent chemotherapy (oxaliplatin and 5-fluorouracil based) and androgen ablation (with triptorelin). The key to management of such a case is early diagnosis and multimodal treatment. The reported survival rate continues to be poor even for a localised disease. A consolidated follow-up protocol ensures early diagnosis of recurrent or metastatic disease so that second-line therapy can be started. Topics: Adenocarcinoma; Antineoplastic Combined Chemotherapy Protocols; Fluorouracil; Genital Neoplasms, Male; Humans; Liver Neoplasms; Male; Middle Aged; Organoplatinum Compounds; Oxaliplatin; Seminal Vesicles; Triptorelin Pamoate | 2017 |
Docetaxel followed by abiraterone in metastatic castration-resistant prostate cancer: efficacy and predictive parameters in a large single center cohort.
To report the outcome and course of disease in patients with metastatic castration-resistant prostate cancer (mCRPC) treated with first-line docetaxel followed by abiraterone acetate in a single center.. In this retrospective observational study, we reviewed the course of disease of all applicable patients with mCRPC treated with docetaxel followed by abiraterone at our center. We analyzed progression-free survival (PFS) of docetaxel and abiraterone treatments. We further searched for predictive factors for the duration of treatment response.. Median PFS between initiation of androgen deprivation therapy and the diagnosis of mCRPC was 32 months. Median PFS on docetaxel treatment was 9 months. Median PFS on abiraterone treatment was 11 months. Patients with higher Gleason scores (GS) (8-10) at initial diagnosis had a significantly longer median PFS on docetaxel as compared to patients with GS 6-7, p = 0.01. We demonstrate a significant correlation between the PFS on docetaxel and PFS on abiraterone in the post-docetaxel setting (Kendall tau r = 0.32, p = 0.019) as well as a significant negative correlation between the PSA nadir under abiraterone treatment and the time to progression under abiraterone (Kendall tau r = -0.43, p = 0.007).. High Gleason score appears to be predictive of duration of response to docetaxel. Interestingly, progression-free survival with abiraterone appears to be correlated with the duration of response with docetaxel, whereas PSA decline and low nadir appear to be predictive of response to abiraterone. Topics: Aged; Androgen Antagonists; Androstenes; Anilides; Antineoplastic Agents, Hormonal; Antineoplastic Combined Chemotherapy Protocols; Bone Neoplasms; Buserelin; Cohort Studies; Disease-Free Survival; Docetaxel; Flutamide; Humans; Leuprolide; Liver Neoplasms; Lung Neoplasms; Male; Middle Aged; Nitriles; Prostatic Neoplasms, Castration-Resistant; Retrospective Studies; Taxoids; Tosyl Compounds; Treatment Outcome; Triptorelin Pamoate | 2015 |
Effect of D-tryptophan-6-luteinizing hormone-releasing hormone on the tumoral growth and plasma sex steroid levels in cirrhotic patients with hepatocellular carcinoma.
Certain evidence suggests androgen dependence of hepatocellular carcinoma in cirrhotic patients. Consequently, it was postulated that antiandrogen therapy might be effective in the treatment of hepatocellular carcinoma. D-Tryptophan-6-luteinizing hormone-releasing hormone is a potent agonist analog of luteinizing hormone-releasing hormone which, when chronically administered, inhibits the pituitary gonadal axis and testicular androgen secretion in man. We studied the effects of D-tryptophan-6-luteinizing hormone-releasing hormone on tumoral growth in 17 male cirrhotic patients with hepatocellular carcinoma. After 3 to 6 months of therapy, no tumoral response was observed. Furthermore, measurements of plasma levels of testosterone, dihydrotestosterone, androstenedione, estradiol, estrone and sex hormone-binding globulin were performed before and 3 months after initiation of the antiandrogenic treatment. Before treatment, hypoandrogenism and hyperestrogenism were present; D-tryptophan-6-luteinizing hormone-releasing hormone induced a fall in plasma testosterone and dihydrotestosterone levels. Only a moderate decrease in estradiol and no modification of plasma estrone and sex hormone-binding globulin were found, indicating that the hyperestrogenemia of cirrhotic patients could be attributed to an increase in peripheral aromatization of androgens of adrenal origin. The inability of D-tryptophan-6-luteinizing hormone-releasing hormone to reduce the growth of hepatocellular carcinoma is not totally in disagreement with the concept of androgen dependence of hepatocellular carcinoma since D-tryptophan-6-luteinizing hormone-releasing hormone does not inhibit the production of androgens of adrenal origin. Topics: Aged; Antineoplastic Agents; Carcinoma, Hepatocellular; Follow-Up Studies; Gonadal Steroid Hormones; Gonadotropin-Releasing Hormone; Humans; Liver Cirrhosis; Liver Neoplasms; Male; Middle Aged; Triptorelin Pamoate | 1989 |