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PURPOSE To report our clinical experience regarding transurethral resection of bladder tumor (TUR-Bt) guided by photodynamic diagnosis (PDD) with intravesical instillations of 5-aminolevulinic acid (ALA) and to assess the usefulness of the therapeutic method. MATERIALS AND METHODS TUR-Bt guided by PDD was performed in 57 patients of which 47 were men and 10 women with a median age of 74.3 years (range 45-90), 36 were primary cases and 21 were recurrent cases with non-muscle invasive bladder cancer. Two to two and half hours prior to endoscopy 1.5 g ALA dissolved in 50 ml of 8.4% sodium hydrogen carbonate (NaHCO3) solution was instilled intravesically. For fluorescence excitation a blue light source (D-LIGHT System, Karl Storz Endoscopy Japan K.K.) was used. The tumorous lesions under white light guidance and the lesion with fluorescent excitation under blue (fluorescence) light guidance were taken by cold cup as a biopsy and also resected sequentially. To evaluate the accuracy of PDD, the levels in images of the ALA-induced fluorescence were compared with the pathological results. To evaluate the availability of TUR-Bt guided by PDD, survival Analysis regarding vesical recurrence was retrospectively examined compared to the cases underwent conventional TUR-Bt under white light guidance. Moreover, in these cases, multivariate analysis using Cox proportional-hazards model was performed to detect the clinico-pathological factor independently contribute to improving prognosis. (Results) In the 301 specimens obtained from 57 patients, the sensitivity and specificity of PDD were 92.5% and 60.1%, whereas the sensitivity and specificity of conventional endoscopic examination under white light guidance were 81.6% and 79.5%, respectively. Median follow-up period was 19.1 (range 8.6-49.9) months in 57 patients underwent TUR-Bt guided by PDD. Eight of 57 patients recurred and recurrence-free survival rate was 88.2 +/- 0.1% (at 12 months) and 76.2 +/- 0.1% (24-48 months). Median follow-up period was 49.9 (5.0-145.0) months in 149 patients underwent conventional TUR-Bt. Ninety-nine of 149 patients recurred and recurrence-free survival rate was 60.3 +/- 0.0% (12 months) and 31.6 +/- 0.0% (24-48 months). There was statistical significance in recurrence-free survival rate between these 2 therapeutic groups (p < 0.001). Moreover, multivariate analysis revealed the independent factor contribute to improving prognosis was only TUR-Bt guided by PDD (hazard ratio 0.279, p = 0.001). CONCLUSION It was suggested that TUR-Bt guided by PDD might reduce the risk of vesical recurrence in the early stage after operation of non-muscle invasive bladder cancer.

To characterize the molecular feature in prostate carcinogenesis and the putative transition from prostatic intraepithelial neoplasia (PIN) to invasive prostate cancer (PC), we analyzed gene-expression profiles of 20 PCs and 10 high-grade PINs with a cDNA microarray representing 23,040 genes. Considering the histological heterogeneity of PCs and the minimal nature of PIN lesions, we applied laser microbeam microdissection to purify populations of PC and PIN cells, and then compared their expression profiles with those of corresponding normal prostatic epithelium also purified by laser microbeam microdissection. A hierarchical clustering analysis separated the PC group from the PIN group, except for three tumors that were morphologically defined as one very-high-grade PIN and two low-grade PCs, suggesting that PINs and PCs share some molecular features and supporting the hypothesis of PIN-to-PC transition. On the basis of this hypothesis, we identified 21 up-regulated genes and 63 down-regulated genes commonly in PINs and PCs compared with normal epithelium, which were considered to be involved in the presumably early stage of prostatic carcinogenesis. They included AMACR, OR51E2, RODH, and SMS. Furthermore, we identified 41 up-regulated genes and 98 down-regulated genes in the transition from PINs to PCs; those altered genes, such as POV1, CDKN2C, EPHA4, APOD, FASN, ITGB2, LAMB2, PLAU, and TIMP1, included elements that are likely to be involved in cell adhesion or the motility of invasive PC cells. The down-regulation of EPHA4 by small interfering RNA in PC cells lead to attenuation of PC cell viability. These data provide clues to the molecular mechanisms underlying prostatic carcinogenesis, and suggest candidate genes the products of which might serve as molecular targets for the prevention and treatment of PC.

Introduction Sarcomatoid carcinoma of the urinary bladder is a rare bidirectional malignant neoplasm with epithelial and mesenchymal differentiation. The epithelial component is mainly high-grade urothelial carcinoma, and the mesenchymal component includes rhabdomyosarcoma. However, proper differential diagnosis of adult rhabdomyosarcomatous tumors of the bladder can be a challenge. Moreover, low-grade urothelial carcinoma as the epithelial component of sarcomatoid carcinoma has not been reported. Case presentation A 64-year-old Asian man with a history of transurethral resection of low-grade urothelial carcinoma of the bladder visited our department with complaints of frequent urination and macroscopic hematuria. Computed tomography and magnetic resonance imaging demonstrated a large mass located in the anterior wall of the bladder. Pathological diagnosis of transurethral biopsy was low-grade, non-invasive papillary urothelial carcinoma, and tumor tissue was removed by total cystectomy. Immunohistochemical studies and fluorescence in situ hybridization assay of the resected neoplastic tissue revealed extensive rhabdomyosarcomatous differentiation causing the formation of a large pedunculated polyp with a papillary appearance of recurrent low-grade urothelial carcinoma. No evidence of recurrence was detected during 2 years of follow-up without further treatment. Conclusions Urothelial carcinoma of the urinary bladder with extensive rhabdomyosarcomatous differentiation is rare, but it should be considered in the differential diagnosis even when urothelial carcinoma coexisting with a rhabdomyosarcomatous component is low-grade and non-invasive.

PURPOSE: We report our technique and also preliminary results in the cases with localized prostate cancer treated by the combination of high-dose rate Iridium-192 (HDR-Ir192) brachytherapy and external irradiation. MATERIALS AND METHODS: From June 1999 to August 2000, 17 patients were treated by the combination of HDR-Ir 192 and external beam. The mean age of patients was 72 years (range, 48-81 years). The clinical stage was B1 in 5, B2 in 7 and C (no cancer with seminal vesicle) in 5 cases. Of 10 patients without neoadjuvant hormonal therapy, the median initial pretreatment PSA was 15.3 ng/ml (6.93-222.32 ng/ml). The treatment was given by HDR-Ir 192 brachytherapy (6 Gy x 3 times/2 days) and external beam irradiation (40 or 45 Gy). The brachytherapy was given using TRUS guided percutaneously inserted temporary needles with a high dose rate remote afterloading control. Local control was evaluated by digital rectal examination. TRUS-guided biopsies and serum PSA evaluations. Follow-up ranged from 2 to 14 months, with a median of 8 months. RESULTS: In 4 (40.0%) of 10 patients without neoadjuvant hormonal therapy the level of serum PSA was decreased to less than 4.0 ng/ml within 3 months after the therapy. The effective grade in the biopsy specimens of 8 patients without neoadjuvant hormonal therapy was Grade Ob in 4, Grade 1 in 1, Grade 3 in 3 cases at 3 months after the therapy. No severe intra- or peri-operative complications occurred. CONCLUSION: The combined radiotherapy treatment is safe and effective for use in the patients with localized prostate cancer. However, more comprehensive studies involving long-term follow-up and great numbers of the cases with localized prostate cancer treated by the combination of HDR-Ir 192 brachytherapy and external irradiation will be necessary to determine whether this therapy contributes to better prognosis.

PURPOSE We tried to improve the materials and methods of high-dose rate Iridium-192 brachytherapy for localized prostate cancer and evaluated the stress during the treatment in 20 patients with whom the therapy was performed. MATERIALS AND METHODS Rigid applicators made of stainless steel of 1.6 mm in diameter were indwelt with a template as usual for 30 hours in 14 patients (group A). Flexible applicators made of polyoxymethylene rosin (POM) of 2.0 mm in diameter were indwelt without a template for 30 hours after the applicator insertion in 6 patients (group B). We made inquiries about lumbago, inconvenience and necessity of assistant help and sleep in the course of therapy, and urinary incontinence and erectile function after the course of therapy as the QOL. RESULTS The stress during the course of therapy in the patients of group B was obviously less than that of group A. There were no significant differences in urinary incontinence and erectile function after the course of therapy between group A and B. CONCLUSION In this study, our trial successfully reduced the stress during the course of therapy in the patients with localized prostate cancer in the course of high-dose rate Iridium-192 brachytherapy.

We used fluorescence in situ hybridization with centromere-specific probes for chromosomes 7, 8, 10, and Y to determine the copy number of these chromosomes in metastatic prostate cancers of five Japanese cases. Freshly prepared samples were obtained from prostate needle biopsies at different phases of clinical treatment; pretreatment, 1 week, 4 weeks, 12 weeks, 24 weeks post-treatment (PT), and clinical relapse. Gain of chromosomes 7 and 8, as noted in pretreatment samples; however, in post-treatment specimens (four of five cases), a remarkable reduction in the number of cells with extra copies of these chromosomes was detected. This decrease in the number of cells with additional chromosome 7 and 8 signals was correlated with the clinicohistopathological findings until 4 weeks PT. Chromosomes Y and 10 did not show numerical aberrations before treatment or changes in cells with aneusomy after treatment in all five cases. Our results suggest that gains of chromosomes 7 and 8 correlate with high grade and stage, and that changes in the cell number with aneusomy of chromosomes 7 and 8 reflect the clinical effects of anti-androgen therapy at an early phase, which may also indicate the androgen dependency of prostate cancer cells.

The object of this study is to evaluate the usefulness of the ATP sensitivity assay for appropriate selection of anticancer drugs for prophylactic bladder instillation therapy in patients with superficial bladder cancer.The ATP assay was performed using the method reported previously. The anticancer drugs examined were ADM, MMC, THP-ADM and EPI. The 5-year rate of non-recurrence in group A (32 cases) which had been treated using the results of ATP assay, was compared with that of group B (37 cases), for which the ATP assay was not performed.The most sensitive anticancer drug was THP-ADM. The 5-year rate of non-recurrence in group A (80.9%) was significantly higher than that in group B (39.4%) (p0.001). Tumor recurrences in group A was observed within 2 years post-operatively in all cases. When the ATP assay was re-performed in 3 cases with recurrent disease, altered antitumor sensitivity was observed.These findings suggested that ATP assay was useful for choosing effective anti-cancer drugs for prophylactic instillation, especially for patients with primary or solitary tumor, grade 2 disease or tumor of a certain size (or = 1 cm). It also appeared that the ATP assay should be performed for patients with primary superficial bladder cancer as a screening test for the selection of drugs for prophylactic instillation therapy.

Extragonadal germ cell tumors are relatively rare tumors, which usually occur in the mediastinum or retroperitoneum. In this report, we present a case of primary seminoma arising in the pelvic cavity. A 58-year-old man with urinary retention and abdominal distension was admitted to our hospital. Computed tomography and magnetic resonance imaging demonstrated a large mass in the pelvic cavity. Histological examination of the specimens obtained by open biopsy revealed seminomatous malignant cells. Immunohistochemical studies detected vimentin, placental alkaline phosphatase and c-kit. Taking these results together with the patient's other clinical manifestations, this case was diagnosed as extragonadal seminoma without c-kit-activating mutations, and chemotherapy followed by radiation therapy was successful. Primary seminoma in the pelvic cavity is extremely rare, but should be considered a cause of pelvic mass formation.

In chromophobe renal cell carcinoma (RCC), two forms of typical and eosinophilic variants have been reported to date. We have previously reported a new variant of chromophobe RCC, namely an oncocytic variant. However, little is known on the histological features of this variant. In this article, we report such five cases. Macroscopically, the tumor was well demarcated, but unencapsulated. The cut surface of the tumor showed brown in color, but neither hemorrhage nor necrosis was seen. Microscopically, the tumor consisted of predominant tubular configuration with or without various proportion of solid-sheet pattern. In one tumor, tumor cells microscopically invaded branches of renal vein. In addition, the constituting cells were characterized by the oncocytic cytoplasm, trivial to minimal variation in tumor size, indistinct to slightly distinct cell border, centrally located round nuclei and the absence of perinuclear halo. These characteristics entirely resembled renal oncocytoma. However, neoplastic cells immunohistochemically showed the diffuse and strong labeling for cytokeratin 7 and mitochondrial antigen in all cases. In addition, in fluorescence in situ hybridization (FISH) study the loss of more than four chromosomes among chromosomes 7, 10, 13, 17 and 21 was confirmed in all tumors and the diagnosis of chromophobe RCC was rendered. In conclusion, we propose a new variant, namely an oncocytic variant, of chromophobe RCC morphologically resembling renal oncocytoma and biologically showing characteristics of chromophobe RCC, and this recognition is practically crucial in the differential diagnosis from renal oncocytoma.

A total of 42 patients with hormone-refractory prostate cancer received E-E therapy. Oral estramustine phosphate (EMP) was administered twice daily for a total daily dose of 560 mg every day and oral etoposide (E-E therapy, 50 mg/body/day) was given on days 1-21 and stopped on days 22-35. Treatment was continued until the disease progression was confirmed radiographically or PSA had increased from base line of at least 25%. The median follow-up period after E-E therapy was 77.4 months (range : 12.5 to 122.3). Nineteen patients (43%) achieved a PSA decrease of 50% or greater. The median survival time of the patients who had a decrease of 50% or greater in the PSA value (PSA responder) was 29.3 months and the patients who did not (PSA non-responder) was 14.1 months (p = 0.01). There were no significant differences between PSA responders and non-responders when taking into account variables. Excluding those patients with only PSA elevation, the survival time was 14.9 months with no significant difference between PSA responders and non-responders. The toxicities (grade 3 or more) were identified as anemia, leukocytopenia thrombocytopenia, cardiovascular events, and gastrointestinal and hepatic disorders, which occurred in 0, 5, 2, 2, 14, and 2% of the patients, respectively. E-E therapy was considered to be an active oral regimen and well-tolerated for outpatients with hormone-refractory prostate cancer in Japanese patients.

A 74-year-old-woman was referred to our hospital for further examination. Her chief complaint had been a high-grade fever, but she was seen at our hospital without fever. Plain film of kidney, ureter and bladder drip infusion pyelography and abdominal computed tomography (CT) showed a gas shadow surrounding calcifications in the right renal pelvis. We diagnosed right emphysematous pyelonephritis. Since changes in the CT findings were not remarkable for 2 weeks, we performed laparoscopic right nephrectomy, even though her condition had not worsened. The renal pelvis contained brownish and clayish matter. We report here this rare case of renal matrix stones.

To characterize the molecular feature in prostate carcinogenesis and the putative transition from prostatic intraepithelial neoplasia (PIN) to invasive prostate cancer (PC), we analyzed gene-expression profiles of 20 PCs and 10 high-grade PINs with a cDNA microarray representing 23,040 genes. Considering the histological heterogeneity of PCs and the minimal nature of PIN lesions, we applied laser microbeam microdissection to purify populations of PC and PIN cells, and then compared their expression profiles with those of corresponding normal prostatic epithelium also purified by laser microbeam microdissection. A hierarchical clustering analysis separated the PC group from the PIN group, except for three tumors that were morphologically defined as one very-high-grade PIN and two low-grade PCs, suggesting that PINs and PCs share some molecular features and supporting the hypothesis of PIN-to-PC transition. On the basis of this hypothesis, we identified 21 up-regulated genes and 63 down-regulated genes commonly in PINs and PCs compared with normal epithelium, which were considered to be involved in the presumably early stage of prostatic carcinogenesis. They included AMACR, OR51E2, RODH, and SMS. Furthermore, we identified 41 up-regulated genes and 98 down-regulated genes in the transition from PINs to PCs; those altered genes, such as POV1, CDKN2C, EPHA4, APOD, FASN, ITGB2, LAMB2, PLAU, and TIMP1, included elements that are likely to be involved in cell adhesion or the motility of invasive PC cells. The down-regulation of EPHA4 by small interfering RNA in PC cells lead to attenuation of PC cell viability. These data provide clues to the molecular mechanisms underlying prostatic carcinogenesis, and suggest candidate genes the products of which might serve as molecular targets for the prevention and treatment of PC.

To search for additional amplification and deletion sites that may serve as a starting point for the discovery of new oncogenes or tumor suppressor genes, 30 Japanese localized prostate cancers were analyzed by comparative genomic hybridization (CGH) in this study. CGH was used to search for changes in DNA sequence copy-number in a series of 30 primary prostate adenocarcinomas, consisting of 22 cases of pT2N0 (organ confined; without capsular invasion) and 8 cases of pT3N0 (with capsular invasion), removed by radical prostatectomy. CGH revealed that the shortest regions of overlap (SRO) of gains in pT2N0 were at 8q22.2 approximately q24.2, 11q13.1 approximately q14.1, and 12q23 approximately q24.2, whereas the SRO of losses were seen at 8p23.3 approximately p22, 13q21.2 approximately p22, and 18q21 approximately q22. The SRO of gains in pT3N0 were noted at 5q32 approximately q34, 8q22.3 approximately q24.1, 11q14.1 approximately q22.3, and 12q22 approximately q24.2, whereas the SRO of losses were seen at 18q21.2 approximately q23. These results suggest that gains or losses of DNA in these regions are important for prostate cancer progression. The detection of the SRO may serve as a starting point to discover novel oncogenes and tumor suppressor genes involved in prostate cancer progression.

In this study, we examined nine cases of advanced Japanese prostate cancer by comparative genomic hybridization (CGH) to detect chromosomal imbalances across the entire genome and to identify several new regions likely to contain genes important to the development and progression of this disease. These cases had been previously examined for numerical chromosomal aberrations by fluorescence in situ hybridization (FISH). By CGH, the following regions were found to be over-represented (gains), with fluorescence ratio values higher than the threshold: 4p, 6p, 8q, 11q, 12q, 15q, 16p, 17q, 20, and 21 (4 cases); underrepresentation (losses) involved: 1q, 4q, 5q, 6q, 13q, 14q, and 22 (4 cases). The shortest regions of overlap (SRO) of gains were noted at 8q24.1 through q24.3, 12q23, and 17q23 through q24 (5 cases). The SRO of losses were seen at 5q14 through q21, 6q16.1 through q21, 13q21.3 through q22, and 14q21 (5 cases). Notably, the gain of chromosomes 8 and 12 by CGH was in agreement with the FISH data, suggesting that the gain of chromosomes 8 and 12 may play an important role in prostate carcinogenesis. The genes on the SRO regions were also discussed in relation to oncogenes and bone metastases.

Publisher Summary This chapter describes the most common techniques of molecular cytogenetics, such as fluorescence in situ hybridization (FISH) and comparative genomic hybridization (CGH), and focuses on their utility in the analysis of prostate cancer. Hereditary and environmental factors play an important role in the development of prostate cancer, but the etiology and risk factors have remained largely obscure. Over the past decades, there has been a rapid increase in understanding of the basic molecular events underlying tumorigenesis. However, the target genes for many of the chromosomal aberrations are not known. Genetic alterations as detected by CGH may not be sufficient for correctly identifying the relevant chromosomal regions important in tumor progression. It is hoped that by recognizing and understanding molecular mechanisms, better tools for the prevention, diagnosis, prognostic evaluation, and treatment of malignancies may be developed. As techniques are improving and examination of archival material is now possible, it should be easier to correlate clinical data with tumor studies. This approach may yield important information for the prognosis of patients with prostate cancer.

Although reduction in the serum prostate specific antigen (PSA) correlates with clinical outcome for high dose rate Iridium-192 (HDR Ir-192) brachytherapy, it takes a long latency period. We investigated numerical chromosome changes of prostatic cancer during the pre- and post-treatment periods of HDR Ir-192 brachytherapy (and external beam radiotherapy), using fluorescence in situ hybridization (FISH) to clear the effect of treatment in early phase. Transitional changes in the frequency of aneuploidy for chromosomes 7, 8, 10, 12, 16, X, and Y in prostate cancer during the pre- and post-treatment periods were observed. Gains of chromosomes 7, 8 and 12 were noted in the pre-treatment samples (4 out of 12 cases in chromosomes 7 and 8; 1 out of 12 cases in chromosome 12), while a notable reduction in the number of cells with extra copies of these chromosomes was observed in post-treatment specimens. This change appears earlier than the reduction in the value of prostate specific antigen (PSA) and strongly reflects the effect of HDR brachytherapy with external beam radiotherapy in localized prostate cancer. Decrease in the number of cells with high ploidies of chromosomes 7, 8 and 12 at 12 weeks after treatment may predict clinical effects of radiation therapy, which may explain the radiation dependency of localized prostate cancer cells.

There have been few detailed studies conducted on the cell population in relation to cytogenetic changes between the pre- and post-treatment periods in patients with prostate cancer. We investigated numerical chromosome changes associated with anti-androgen therapy, using fluorescence in situ hybridization (FISH). FISH using chromosome-specific centromeric probes was used to assess transitional changes in the frequency of aneuploidy for chromosomes 7, 8, 10, 12, 16, X, and Y in prostate cancer during the pre- and post-treatment periods. Gains of chromosomes 7, 8 and 12 were notable in the pre-treatment samples (8 out of 9 cases in chromosome 7; 8 out of 9 cases in chromosome 8; 7 out of 9 cases in chromosome 12), while a notable reduction in the number of cells with extra copies of these chromosomes was observed in post-treatment specimens. Other chromosomes did not show noticeable change in their FISH signals at each phase of clinical treatment in all 9 cases. Changes in cell number with high ploidies of chromosome 7, 8 and 12 reflect the clinical effects of anti-androgen therapy at the early phase, which might explain the androgen dependency of metastatic prostate cancer cells.

Primary adenocarcinoma of the urinary bladder has shown an extremely poor response to radiation or chemotherapy. Therefore, radical surgery is the only therapeutic treatment for it. A case report is presented of a primary advanced adenocarcinoma of the urinary bladder invaded into the uterus with distant metastases which responded completely to systemic combination chemotherapy including tegafur-uracil. The patient was a 53-year-old woman with a history of asymptomatic macrohematuria. She was treated with the combination of cisplatinum, mitomycin-C, etoposide and tegafur-uracil chemotherapy. After four courses of the chemotherapy, computed tomography showed marked regression of the primary tumor of the urinary bladder and the complete disappearance of the distant metastases in the liver, lung and para-aortic lymph node. Subsequently, she underwent radical cystectomy and cutaneous ureterostomy. Pathologically, no viable cancer cells were detected. Three years after the operation, she has no evidence of disease recurrence. Treatment of advanced adenocarcinoma of the urinary bladder by this combination chemotherapy is of benefit.

Background: We previously reported favorable results of intraarterial doxorubicin chemotherapy in combination with low-dose radiotherapy for locally-advanced bladder cancer. We have now designed a new intraarterial chemotherapy regimen to achieve a higher tumor response rate while preserving a functional bladder. Methods: Twenty-one patients with muscle-invasive bladder cancer (T2, lO; T3,7; T4,4) were treated with concurrent intraarterial chemotherapy and radiotherapy after an initial complete transurethral resection. Induction therapy consisted of concomitant pirarubicin (THP; 15 mg/m2/day on days 1 to 3), cisplatin (CDDP; 25 mg/m2/day on days 8 to 10) and irradiation (2 Gy/session on days 1 to 3 and 8 to 10). Maintenance treatment consisted of THP administered at 20 or 30 mg with or without 50 mg CDDP every month for 2 years. Results: Nineteen of the 21 patients (90.5|X%) achieved a complete response (CR). One of these 19 relapsed with lung metastases 24 months after treatment and was treated surgically. The 2 patients who did not achieve a CR died of cancer, while the remaining 19 patients are alive with preservation of a functional bladder. Conclusion: These findings suggest that a higher tumor response rate with bladder preservation for patients with muscle-invasive bladder cancer is achieved by intraarterial THP/CDDP chemotherapy plus radiotherapy.

BACKGROUND The objective of this study is to evaluate the usefulness of intra-arterial chemotherapy using an implantable injection system for the treatment of bladder or prostate cancer. METHODS Twenty-four patients with bladder cancer and 13 with prostate cancer were treated with intermittent intra-arterial chemotherapy using a totally implantable injection pump. A heparinized catheter was percutaneously fixed through the femoral artery with the tip 2 or 3 cm above the bifurcation of the common iliac artery, and the pump was placed in a subcutaneous pocket. RESULTS The total number of infusion sessions for bladder cancer ranged from 4 to 38 times (mean 20.8), and 15 of the 24 patients were injected from 2 to 19 sessions (mean 8.5) as outpatients. The tumor response for 15 patients with newly diagnosis muscle-invasive bladder cancer were 12 patients in CR, 1 in PR, and 2 in NC, and 9 patients with recurrent bladder cancer were 6 patients in CR, 1 in PR, and 2 in NC. The total number of infusions for prostate cancer ranged from 6 to 35 times (mean 20.2), and 10 of the 13 patients were injected from 1 to 11 times (mean 6.3) as outpatients. All 13 patients with prostate cancer were treated with hormone therapy and irradiation, and achieved PR. Complications of this drug delivery system were obstruction of the catheter or pump observed in 7 patients, dislocation of the catheter in 2, and obstruction of right external iliac artery in 1. CONCLUSION These findings suggest that favorable therapeutic efficacies and an improved quality of life for patients can be obtained by intra-arterial chemotherapy using an implantable injection pump.