A total of 20 patients with hormone-refractory prostate carcinoma entered a pilot study of combination chemotherapy based on the EAP (etoposide, Adriamycin and cisplatin) regimen, in which Adriamycin was replaced by pirarubicin, a less cardiotoxic derivative of Adriamycin. The response was assessed by criteria modified from those of the National Prostatic Cancer Project: prostate-specific antigen was employed instead of acid phosphatase. Of 18 evaluable patients, 6 achieved a partial response, 5 had stable disease, and in 7 the disease had progressed during therapy; thus, the overall response rate was 33.3% [95% confidence interval (CI) 11.5-55.1%]. Significant pain alleviation and performance status improvement were obtained in 5 of 12 patients (41.7%; CI 13.8-69.6%) and 3 of 13 patients (23.1%; CI 0.2-46.0%), respectively. Although myelosuppression was moderate to severe, no chemotherapy-related deaths or bacteriologically documented sepsis occurred; nor was there any clinical cardiotoxicity. All the responding patients received maintenance chemotherapy with etoposide thereafter. At present, the median duration of response is 33 weeks (range: 23-91 weeks) and the median survival period for all patients is 42 weeks (range: 27(+)-136 weeks), with 12 deaths. In spite of the small number of patients treated, these results suggest that this chemotherapy regimen is active in advanced hormone-refractory prostate carcinoma.

Download full-text PDF

Source
http://dx.doi.org/10.1007/BF00686552DOI Listing

Publication Analysis

Top Keywords

hormone-refractory prostate
12
prostate carcinoma
12
advanced hormone-refractory
8
weeks range
8
patients
7
treatment advanced
4
carcinoma combination
4
combination etoposide
4
etoposide pirarubicin
4
pirarubicin cisplatin
4

Similar Publications

EphB4-ephrin-B2 are targets in castration resistant prostate cancer.

Br J Cancer

March 2025

Department of Medicine, USC Norris Comprehensive Cancer Center, Keck School of Medicine, University of Southern California, Los Angeles, CA, USA.

Background: PI3K pathway activation is a common and early event in prostate cancer, from loss of function mutations in PTEN, or activating mutations in PIK3Ca or AKT leading to constitutive activation, induction of growth factor-receptors kinase EphB4 and its ligand ephrin-B2. We hypothesized that induction of EphB4 is an early event required for tumor initiation. Secondly, we hypothesized that EphB4 remains relevant when prostate cancer becomes androgen independent.

View Article and Find Full Text PDF

Radiation therapy (RT) is the cornerstone treatment for prostate cancer; however, it frequently induces gastrointestinal and genitourinary toxicities that substantially diminish the patients' quality of life. While many individuals experience transient side effects, a subset endures persistent, long-term complications. A promising strategy to mitigate these toxicities involves enhancing tumor radiosensitivity, potentially allowing for lower radiation doses.

View Article and Find Full Text PDF

A 79-year old Caucasian male with metastatic hormone refractory prostate cancer and bilateral nephrostomy was admitted to the emergency department due to 4-day bloody urethral discharge, weakness and dizziness. The patient was treated with the luteinizing hormone-releasing hormone-antagonist and abiraterone acetate plus prednisone, dabigatran 150 mg bid (for atrial fibrillation and coronary heart disease) and 5-aminosalicylic acid for the management of mild ulcerative colitis. Imaging revealed bladder overdistention and blood analysis low levels of hematocrit (HCT) and hemoglobin (HGB) (HCT, 22%; HGB, 7.

View Article and Find Full Text PDF

Prostate cancer is a leading cause of cancer-related morbidity and mortality in men, frequently exhibiting resistance to conventional anti-androgen therapies. This review investigates the emerging significance of the aryl hydrocarbon receptor (AhR) in prostate cancer, focusing on its role in modulating androgen receptor (AR) signaling and its potential as a therapeutic target. AhR, traditionally known for detoxifying harmful compounds, has been increasingly recognized for its dual capacity to either enhance or inhibit AR activity based on cellular context and specific coactivators.

View Article and Find Full Text PDF

Estramustine (EM), a clinically successful hormone-refractory anti-prostate cancer drug, exhibited potent anti-proliferative activity, depolymerized microtubules, blocked cells at mitosis, and induced cell death in different cancer cells. Altered iron metabolism is a feature of cancer cells. Using EM, we examined the plausible relationship between microtubule depolymerization and induction of ferroptosis in human neuroblastoma (SH-SY5Y and IMR-32) cells.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!