Primary choriocarcinoma of the renal pelvis presenting as intracerebral hemorrhage: a case report and review of the literature.

INTRODUCTION: A choriocarcinoma is a malignant neoplasm normally arising in the gestational trophoblast, gonads and, less frequently, the retroperitoneum, mediastinum and pineal gland. Primary choriocarcinomas of the renal pelvis are extremely rare. CASE PRESENTATION: We report a case of primary choriocarcinoma of the renal pelvis in a 38-year-old Greek woman of reproductive age, presenting with a sudden development of intracerebral hemorrhage due to metastatic lesions. The diagnosis was established with a renal biopsy, along with an elevated serum level of beta-human chorionic gonadotropin. An extensive diagnostic work up confirmed the origin of the choriocarcinoma to be the renal pelvis. CONCLUSION: Extragonadal choriocarcinomas are rare neoplasms that require extensive laboratory and imaging studies to exclude a gonadal origin. Moreover, this is the first case of severe intracerebral hemorrhage as the initial presentation of primary choriocarcinoma of the renal pelvis. Nonetheless, choriocarcinomas should be considered in the differential diagnosis of women of reproductive age.

Myelotoxicity of oral topotecan in relation to treatment duration and dosage: a phase I study.

Oral topotecan has been recently brought into clinical practice at a dose of 2.3 mg/m(2) for 5 days, every 3 weeks. Published data show quite high myelotoxicity. The aim of this trial was to define the daily dose and treatment duration, which permits safe toxicity. The study was designed to begin at a low daily dosage of 1.5 mg/m(2) and was escalated by increasing the topotecan dose and the day-treatment duration. The plan was to end up with 2.3 mg/m(2) daily for 5 days. In cases of tolerability with the last dosage given, we would then continue testing a higher daily dosage. Treatment repetition was planned to be every 21 days. Dosage levels were 1.5, 2.0 and 2.3 mg/m(2) for 3 days, 2.0 and 2.3 mg/m(2) for 4 days, and 2.3 mg/m(2) for 5 days. Toxicity was scored according to the Common Toxicity Criteria. Thirty-two patients (27 male, five female, median age 60 years, range 46-77 years) with small-cell lung cancer were included. The patients on 1.5 and 2 mg/m(2) for 3 days showed no myelotoxicity. Four (25%) patients on 2.3 mg/m(2) 3-day treatment developed grade 3-4 neutropenia. Three of five patients (60%) treated for 4 days at a dose of 2.3 mg/m(2) developed grade 3-4 neutropenia and less than half (two of five, 40%) of these patients had thrombocytopenia. Eight patients (66.7%) on the 5-day treatment presented with serious grade 3-4 myelotoxicity. Two treatment-related deaths were observed in the 5-day group and one in the 4-day group. Granulocyte growth factor was applied in over 60% of the patients. In conclusion, a dose of 2.3 mg/m(2) for 5 days was intolerable. Dose-limiting toxicity was 2.3 mg/m(2) for 4 days without prophylactic granulocyte colony-stimulating factor administration. The safe duration of oral topotecan treatment and the maximum tolerated dose seem to be not longer than 3 days at a dose of 2.3 mg/m(2).

Survival after cytotoxic chemotherapy in patients with advanced hormone-resistant prostate cancer: a phase II study.

In the past, it was believed that when advanced-stage prostate cancer became resistant to hormonal management, no chemotherapy should be administered, as survival was not prolonged. Mitoxanthrone and prednisone were mostly administered, while recently, other agents such as docetaxel or paclitaxel have been tested both with and without hormonal treatment. The objective of the present phase II study was to determine the survival and the response rate of patients after the chemotherapy was administered. Sixty-five patients with advanced prostate cancer were included. The inclusion criteria involved histological confirmation of adenocarcinoma and resistance to hormonal therapy. The majority of the patients had stage IVa or IVb disease and a performance status of 0-1 to 2. The treatment involved chemotherapy in combination with a luteinizing hormone-releasing hormone (LHRH) or dexamethasone or estramustine. The hormone treatment preceded the cytotoxic administration and no amelioration in the patients nor prostate serum antigen (PSA) reduction was observed. The initial cytotoxic agents administered were docetaxel 75 mg/m(2) in 25 patients, mitoxanthrone 10 mg/m(2) in 15 patients, epirubicin 75 mg/m(2) in 15 patients and paclitaxel 175 mg/m(2) in 10 patients, all repeated every 3 weeks. The response rate was documented by bone scan, CT scan of the abdomen (and occasionally of the chest) and by the PSA serum value. Clinical benefit was also estimated. Thirty-three (50.77%) patients achieved a partial response; stable disease was observed in 24 (36.92%) patients and disease progression in 8 (12.31%). Twenty-two (33.85%) experienced clinical benefit. A significant PSA reduction was seen in 35 (53.85%) patients. The median survival was 18 months and the range 3-84 months. One, 2, 3 and five-year survival was 75.38, 23.07, 12.30 and 4.66%, respectively. Toxicity was well-tolerated. Patients with hormone-resistant advanced prostate cancer do have good prospects for receiving substantial benefit with the addition of chemotherapy, as observed in the present trial.

First-time use of bevacizumab for aggressive, metastatic hepatocellular carcinoma in an HIV/hepatitis B virus coinfected patient: a case report.

We present a case of an HIV-1 infected patient with history of chronic hepatitis B and chronic alcohol use without cirrhosis, who presented with aggressive hepatocellular carcinoma with multiple metastases. Systemic chemotherapy combined with use of bevacizumab (anti-vascular endothelium growth factor monoclonal antibody) was without effect and the patient succumbed to his disease within few weeks. To our knowledge, this is the first report in the English literature of bevacizumab use for metastatic hepatocellular carcinoma in HIV-infected patients.

Prognostic implications of the immunohistochemical expression of human kallikreins 5, 6, 10 and 11 in renal cell carcinoma.

Human kallikreins 5, 6, 10 and 11 (hK5, 6, 10 and 11) are expressed by many normal tissues, and it has been suggested that they may represent candidate tumor-diagnostic or -prognostic markers. In patients with renal cell carcinoma (RCC), outcome is unpredictable despite the use of conventional prognostic factors. The aim of this study is to evaluate the immunohistochemical expression and the prognostic value of the above kallikreins in RCC. The study comprised 95 patients who underwent radical nephrectomy for RCC. The median follow-up period was 60 months (range 1-180 months). Fifty-seven RCC cases were immunostained for hK5, 70 for hK6, 70 for hK10 and 69 for hK11. The streptavidin-biotin-peroxidase method of immunostaining was performed using anti-hK5, anti-hK6, anti-hK10 and anti-hK11 monoclonal and polyclonal antibodies. The immunohistochemical expression of these kallikreins was correlated with tumor size, histological type, histological malignancy according to the Fuhrman four-grade scale, mitotic index, pathological stage and disease survival. For the statistical analysis, four grades were collapsed into two by which RCC cases were categorized as low malignant (LM) and high malignant (HM). In the normal renal parenchyma adjacent to the tumors, the renal tubular epithelium showed a cytoplasmic expression of all four kallikreins. In RCC, immunohistochemical expression was decreased: 33 of 57 cases (58%) were positive for hK5, 27 of 70 (39%) for hK6, 46 of 70 (66%) for hK10 and 32 of 69 (46%) for hK11. A statistically significant positive correlation was observed among the immunohistochemical expression of all kallikreins. HM-RCC expressed all kallikreins in a higher percentage of cases than LM-RCC, but statistically significant differences were only observed for hK6 and hK10 (55 vs. 27%, p = 0.016, and 79 vs. 56%, p = 0.044, respectively). hK6 and hK11 expression showed a positive correlation to pathological stage: hK6 with both Robson and TNM 2002 staging systems (p = 0.010 and p = 0.017, respectively), and hK11 only with the Robson staging system (p = 0.045). In both the Kaplan-Meier and the univariate Cox regression analyses, hK6 expression was negatively correlated with disease-specific survival (p = 0.05 and p = 0.038, respectively). In univariate analysis, nuclear grade, Robson stage and TNM stage also correlated with disease-specific survival. However, in the multivariate analysis, TNM stage was the only independent prognostic factor. In conclusion, although the immunohistochemical expression of hK5, hK6, hK10 and hK11 was downregulated in RCC, tumors of high grade and late stage expressed one or more of the above kallikreins in a higher percentage of cases, and hK6 may predict a poor disease outcome in RCC.

Prostate cancer with small-cell morphology: an immunophenotypic subdivision.

OBJECTIVE: To study the immunophenotypic characteristics and clinical outcome of morphologically undifferentiated prostatic carcinoma with small-cell morphology (U-PC-SCM). MATERIAL AND METHODS: Sixteen patients with U-PC-SCM were enrolled. The streptavidin-biotin complex immunohistochemical method was used on paraffin-embedded tissue sections to test positivity for prostate-specific antigen, prostate-specific acid phosphatase, CD57, androgen receptors, CK8-18, epithelial membrane antigen, carcinoembryonic antigen, CD56, neuron-specific enolase, chromogranin, synaptophysin, serotonin, various hormones, thyroid transcriptional factor-1 and Ki-67/MIB1. RESULTS: Based on immunophenotypic criteria, we identified two groups of patients. The final diagnosis was U-PC (Gleason score 10) in Group 1 (n=9) and pure or mixed neuroendocrine small-cell carcinoma in Group 2 (n=7). Group 1 underwent total androgen blockade (TAB) with no major response and had a median survival of 9 months. In Group 2, three patients underwent TAB, two of whom died of progressive disease. The third patient showed a partial response (PR) for 18 months but eventually relapsed with liver metastatic lesions. He was then treated with cisplatin + etoposide and showed a PR for 3 months and survived for 5 months after the initiation of the second-line chemotherapy (CTH) treatment. The other four patients received six cycles of cisplatin + etoposide. There were two complete responses of >14 and >22 months, respectively and 2 PRs of 11 and 17 months, respectively, the partial responders surviving for 14 and 21 months, respectively. CONCLUSION: U-PC-SCM with a neuroendocrine immunophenotype is a histogenetically distinct entity with different clinical and laboratory manifestations which responds well to a cisplatin + etoposide CTH regimen.

Tumor to tumor metastasis: report of two cases and review of the literature.

Tumor-to-tumor metastases are uncommon. The most frequent donor tumor is lung cancer, while renal cell carcinoma (RCC) is by far the most common recipient. In this report, a carcinoma of the uterine cervix metastasizing to an RCC and a urothelial carcinoma of the urinary bladder metastasizing to a solitary fibrous tumor of the pleura are described. No similar cases have been found in the accessible literature. These cases are discussed and the findings are correlated with the data of the literature.