amrubicin and Prostatic-Neoplasms

This study retrospectively reviewed the clinical characteristics and treatment outcomes of patients with histologically diagnosed treatment-related pure small-cell neuroendocrine prostate cancer.. We retrospectively evaluated data for 13 patients with treatment-related neuroendocrine prostate cancer who were diagnosed between May 2015 and February 2022. Standardized systemic therapies of etoposide plus cisplatin (or carboplatin), amrubicin and nogitecan were selected as sequential treatments. Cancer-specific survival and progression-free survival were evaluated as the primary endpoint. The Cox proportional hazards model was used to evaluate the relationships between treatment regimens, clinical variables, cancer-specific survival and progression-free survival.. The median cancer-specific survival after diagnosis for all patients was 22.4 months (range 1.3-33.4 months). The median progression-free survival was 9.3 months after first-line etoposide plus cisplatin (or carboplatin) treatment (n = 13); 4.2 months after second-line amrubicin treatment (n = 4); and >15 months after third-line nogitecan treatment (n = 2). The median progression-free survival after first-line chemotherapy of the liver metastasis (-) group was 10.2 months, and that of the (+) group was 5.3 months (P = 0.015, hazard ratio = 11.6, 95% confidence interval = 1.01 - 133.7). No clinicopathological parameters were identified as significant independent predictors of cancer-specific survival in univariate analysis.. Sequential chemotherapy with etoposide plus cisplatin (or carboplatin), amrubicin and nogitecan may be helpful for patients with treatment-related pure small-cell neuroendocrine prostate cancer. Early biopsy of metastases and initiation of effective therapy is essential for patients with progressive castration-resistant prostate cancer and low prostate-specific antigen.

Topics: Antineoplastic Combined Chemotherapy Protocols; Carboplatin; Cisplatin; Etoposide; Humans; Lung Neoplasms; Male; Prostatic Neoplasms; Retrospective Studies; Small Cell Lung Carcinoma; Treatment Outcome

Topics: Aged; Anthracyclines; Antineoplastic Agents; Carcinoma, Small Cell; Drug Resistance, Neoplasm; Humans; Male; Middle Aged; Platinum; Prognosis; Prostatic Neoplasms

A 68-year-old man was diagnosed with prostate cancer (initial serum prostate specific antigen [PSA] 389 ng/ml, stage cT4N1M1c, Gleason score 5+4), and androgen deprivation therapy was initiated. Despite the low serum PSA level, he developed postrenal acute kidney failure 4 years later, with progression of prostate cancer and liver and lung metastases. Serum levels of neuron-specific enolase and pro-gastrinreleasing peptide (tumor markers) were elevated. He underwent re-biopsy of the prostate, and histopathological examination revealed small cell carcinoma. He was initially treated with carboplatin and etoposide therapy. Liver metastases showed partial remission, and serum tumor marker levels were temporarily reduced. However, disease progression was observed after 4 chemotherapy cycles, and he was then treated with an 8-cycle course of amrubicin. Metastases showed shrinkage, and serum tumor marker levels were reduced after 2 chemotherapy cycles. Tumor enlargement recurred after 8 cycles, and the patient is being treated with palliative therapy. Amrubicin therapy may be effective in the treatment of small cell carcinoma of the prostate.

Topics: Aged; Androgen Antagonists; Anthracyclines; Carcinoma, Small Cell; Humans; Male; Neoplasm Recurrence, Local; Prostate-Specific Antigen; Prostatic Neoplasms

Small cell carcinoma of the prostate (SCCP) is rare, and no standard treatment regimen has yet been established. The overall prognosis remains poor. We experienced a case who obtained relative long-term survival with two types of chemotherapy treatments. A 69-year-old man underwent combined androgen blockade (CAB) with a diagnosis of prostate adenocarcinoma (Gleason score = 5 + 3) that was staged T3bN1M1b (initial PSA = 352 ng/ml). Twenty-five months after hormonal therapy, the level of serum PSA had elapsed remain low, however, FDG-PET/CT revealed high value at the lymph node of para-aortic and pelvic lesion. The levels of serum NSE and Pro-GRP elevated, and a prostate re-biopsy revealed a small cell carcinoma. Therefore, he was treated with 12-cycles of combination chemotherapy consisting of etoposide and carboplatin. Then, disease has progressed, so he was changed to second line chemotherapy with amrubicin. He underwent 12-cycles chemotherapy with amrubicin, but he died of cancer 39 months after the initial treatment of SCCP.

Topics: Aged; Anthracyclines; Antineoplastic Agents; Carboplatin; Carcinoma, Small Cell; Etoposide; Fatal Outcome; Humans; Lymphatic Metastasis; Male; Multimodal Imaging; Positron-Emission Tomography; Prostatic Neoplasms; Time Factors; Tomography, X-Ray Computed

We describe the use of amrubicin hydrochloride to treat small cell carcinoma of the prostate in a 23-year-old man. Initial radiological examinations of the patient revealed a pelvic tumor associated with bilateral hydronephrosis, pelvic lymph node swelling, and lumbar vertebral bone metastases. The pathological diagnosis was small cell carcinoma originating in the prostate, based on positive immunohistochemical staining for neuron-specific enolase, synaptophysin, and myoglobulin; and negative staining for CD3e, CD20, leukocyte common antigen, and CD99. The clinical stage was T4N1M1. A bilateral nephrostomy was performed to improve renal function, and an ileostomy was established to prevent ileus. The first induction chemotherapy consisted of amrubicin 35 mg/m(2) (days 1, 2, 3, monthly). The amrubicin regimen caused a dramatic reduction in tumor size, but could not be continued, because of the occurrence of grade 4 diarrhea. A different regimen was then administered, consisting of one cycle of a 50% dose and a second cycle of a 75% dose of etoposide (100 mg/m(2) days 1, 2, 3), coadministered with carboplatin (AUC 5, plasma concentration curve). Five months after the induction of chemotherapy, the patient suffered respiratory arrest and died.

Topics: Adult; Anthracyclines; Antineoplastic Agents; Bone Neoplasms; Carcinoma, Small Cell; Humans; Hydronephrosis; Male; Pelvic Neoplasms; Prostatic Neoplasms

Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) induces apoptosis in various tumor cells. The anthracycline doxorubicin (DOX) can sensitize several types of cancer cells to TRAIL-mediated apoptosis. Here we report that DOX enhances TRAIL-induced apoptosis and cytotoxicity against prostate cancer cells. Cytotoxicity was determined by a MTT assay. Synergistic effect was assessed by isobolographic analysis. Caspase activity was determined by a quantitative colorimetric assay. The combination treatment with DOX and TRAIL resulted in a synergistic cytotoxic effect on LNCaP, LNCaP-Bcl-2, PC-3, and PC93 human prostate cancer cell lines, but not on normal human prostatic stromal cells. Synergistic cytotoxicity was also obtained even when the exposure time was shortened from 24 to 8 or 2 h. A similar effect was achieved with TRAIL in combination with epirubicin, pirarubicin, or amrubicin. The synergy obtained in cytotoxicity with TRAIL and DOX was also achieved in apoptosis. DOX treatment significantly activated caspase-8, -6, and -3 in LNCaP cells. Furthermore, the synergistic cytotoxicity of TRAIL and DOX was completely inhibited by Z-VAD-FMK, and partly inhibited by Ac-IETD-CHO, Ac-DQTD-CHO, or Ac-DMQD-CHO. These findings indicate that DOX enhances TRAIL-induced apoptosis and cytotoxicity in prostate cancer by activation of caspase cascades, and suggest that TRAIL in combination with DOX have a therapeutic potential in the treatment of prostate cancer.

Topics: Acridine Orange; Anthracyclines; Antibiotics, Antineoplastic; Apoptosis; Apoptosis Regulatory Proteins; Caspase 3; Caspase 6; Caspase 8; Caspase 9; Caspases; Coloring Agents; Dose-Response Relationship, Drug; Doxorubicin; Epirubicin; Humans; Immunohistochemistry; Male; Membrane Glycoproteins; Prostatic Neoplasms; Recombinant Proteins; Tetrazolium Salts; Thiazoles; Time Factors; TNF-Related Apoptosis-Inducing Ligand; Tumor Cells, Cultured; Tumor Necrosis Factor-alpha