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BACKGROUND: Transitional cell carcinoma (TCC) has recently been acknowledged as a distinct histologic pattern of the uncommon primary fallopian tube carcinoma. However, rare cases of TCC that are closely associated to the extraluminal portion of the tube remain widely unrecognized. CASE: We present a left adnexal high-grade TCC in a 56-year-old postmenopausal woman with an elevated serum CA-125 level. The tumor was attached by a small stalk to the serosal surface of the left fallopian tube and was completely separate from the uninvolved uterus and ipsilateral ovary. Histologic examination of the tubal lumen epithelium revealed neither atypia nor involvement by the neoplasm. Immunohistochemistry showed the tumor cells to be positive for pankeratin, calretinin, progesterone and estrogen receptors, and cytokeratin 7, and negative for cytokeratin 20, consistent with a Mullerian derivation. CONCLUSION: Our case represents the fourth reported instance of a primary paratubal TCC. Perhaps, this entity falls under a previously unrecognized category of carcinomas that collectively may arise from Walthard's rest, paratubal cyst, or directly from the tubal serosa.
PURPOSE: Transitional cell carcinoma (TCC) is a pan-urothelial disease characterized by multiplicity. Although little is known about the molecular events in upper-tract TCC, similar carcinogenic mechanisms are thought to occur throughout the urinary tract. However, we have previously shown that distinct patterns of microsatellite instability occur in upper and lower urinary tract TCC, suggesting biologic differences between these tumors. Here we investigate the extent of promoter hypermethylation in TCC throughout the urinary tract. PATIENTS AND METHODS: Tissue was obtained from 280 patients (median follow-up, 56 months) whose tumors comprised 116 bladder and 164 upper-tract tumors (UTT). Analysis for hypermethylation at 11 CpG islands, using methylation-sensitive polymerase chain reaction and bisulfite sequencing, was performed for each sample and compared with the tumor's clinicopathologic details, microsatellite instability status, and subsequent behavior. RESULTS: Promoter methylation was present in 86% of TCC and occurred both more frequently and more extensively in UTT (94%) than in bladder tumors (76%; P < .0001). Methylation was associated with advanced tumor stage (P = .0001) and higher tumor progression (P = .03) and mortality rates (P = .04), when compared with tumors without methylation. Multivariate analysis revealed that methylation at the RASSF1A and DAPK loci, in addition to tumor stage and grade, were associated with disease progression (P < .04). CONCLUSION: Despite morphologic similarities, there are genetic and epigenetic differences between TCC in the upper and lower urinary tracts. Methylation occurs commonly in urinary tract tumors, may affect carcinogenic mechanisms, and is a prognostic marker and a potential therapeutic target.
Advanced transitional cell carcinoma (TCC) of the urothelial tract is usually fatal despite high response rates to platinum-based chemotherapy regimens. Paclitaxel (Taxol; Bristol-Myers Squibb Company, Princeton, NJ) has demonstrated marked single-agent activity in TCC, and combinations of carboplatin and paclitaxel have been well tolerated in other solid tumors. Methotrexate is also active in TCC. Due to unexpectedly severe myelosuppression and mucositis when methotrexate and paclitaxel were combined, we undertook a phase I trial of paclitaxel, carboplatin, and escalating doses of methotrexate with granulocyte colony-stimulating factor and leucovorin support in advanced TCC to determine the feasibility of this combination. Nineteen previously untreated patients with locally advanced or metastatic TCC were eligible. Median age was 62 years. In sequence, paclitaxel 200 mg/m2 (3-hour infusion), carboplatin dosed to an area under the concentration-time curve of 6 mg/mL x min, and methotrexate 10 mg/m2, increasing in 10-mg/m2 increments, were administered on day 1 every 21 days. Granulocyte colony-stimulating factor 300 microg/d or 480 microg/d (in patients <60 kg or >60 kg, respectively) was administered on days 2 through 11 and leucovorin 15 mg orally every 6 hours for 3 days. At this time, the methotrexate dose has been escalated to 50 mg/m2. There were no dose-limiting toxicities in cycle 1. Sixty-eight cycles have been administered (range, one to eight cycles; median, three cycles). Significant hematologic toxicity including neutropenic sepsis (two episodes) occurred in subsequent cycles, but was infrequent. The major nonhematologic toxicity was neuropathy. Sixteen patients are evaluable for response. One patient has achieved a complete response, seven are partial responders, seven have stable disease, and one progressed on therapy. The overall response rate is 50% (95% confidence interval, 25% to 75%). The combination of paclitaxel, carboplatin, and methotrexate holds promise to be well tolerated and active in advanced TCC.
PURPOSE: Transitional cell carcinoma (TCC) of the urinary tract is a chemosensitive tumor. Most deaths from TCC of the urinary tract are caused by metastasis, which is resistant to conventional chemotherapy. Frequent sites of metastases from TCC of the urinary tract are regional lymph nodes, liver, lung, and bone. Of these distant metastases, bone metastasis is consistently resistant to cisplatin-based conventional chemotherapy. Therefore, in this study, we investigated whether or not a newly developed minodronate, YM529, could prevent osteolytic bone metastasis of human TCC and also enhance the effect of docetaxel in a bone tumor model of athymic nude mice. EXPERIMENTAL DESIGN: In the present study, we evaluated the effect of in vitro treatment with minodronate and/or docetaxel on the proliferation by cell count, the induction of apoptosis by terminal deoxynucleotidyl transferase-mediated nick end labeling (TUNEL) assay, and the biological activity of osteoclast by pit formation assay in human bladder cancer cell line, UMUC-14, and mouse osteoclast cells. In vivo, we examined the effect of minodronate in a bone tumor model of athymic nude mice, in which the percutaneous intraosseal injection in the tibia of UMUC-14, leads to osteolytic bone tumor, as a bone metastasis model. To examine whether or not minodronate could inhibit tumorigenicity and enhance the effect of the chemotherapeutic agent, docetaxel, we gave minodronate i.p. and/or docetaxel i.p. to nude mice 3 days after an intraosseal tumor implantation. Moreover, proliferation and the induction of apoptosis of cancer cells and osteoclasts in bone tumors were determined by immunohistochemistry and the TUNEL assay. RESULTS: In vitro: In vitro treatment with docetaxel inhibited proliferation and resorption pit-forming activity and induced apoptosis of mouse osteoclast cells and UMUC-14 cells. In vitro treatment with minodronate inhibited proliferation and activity and induced apoptosis of mouse osteoclast cells but not UMUC-14 cells. The treatment with minodronate enhanced the inhibition of proliferation and activity by docetaxel in osteoclasts. In vivo: In vivo combination therapy with docetaxel and minodronate significantly reduced the tumor incidence compared with the control (P < 0.05) and also growth of intraossal TCC in athymic nude mice compared with the control (P < 0.001), single therapy with docetaxel (P < 0.01), and minodronate (P < 0.05). Drug-induced body weight loss was not significantly different in any treatment group. Therapy with minodronate significantly enhanced inhibition of proliferation by docetaxel in osteoclasts of bone tumors compared with the control (P < 0.01), single therapy with docetaxel (P < 0.01), and minodronate (P < 0.05). CONCLUSIONS: These studies indicate that combination therapy with minodronate and docetaxel may be beneficial in patients with bone metastasis of human TCC in the urinary tract.
OBJECTIVES: We report a new case of simultaneous renal cell adenocarcinoma and ipsilateral multifocal transitional cell carcinoma. METHODS: 73-year-old man with initial diagnosis of transitional cell carcinoma of the urinary tract whose pathological report showed a asynchronous renal cell carcinoma. RESULTS: We present microphotographs of both tumors after radical surgery. CONCLUSIONS: The presentation of both tumors in the same kidney is unusual, although there are around 47 cases in the bibliography worldwide, 8 of them in Spanish. Presentation of both tumors altogether does not worsen prognosis.
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Transitional cell carcinoma of the urethra in men after radical cystectomy for bladder carcinoma have an incidence which varies from 4 to 18%. The Authors present their experience of 6 cases (6/196; 3.06%) analysing the characteristics of the urethral neoplasm and confirming the systematic cystourethrectomy when there is a urethra prostatic and bladder neck infiltration or when there is a urethral ca in situ. It also underlines the role of the clinical, radiological, cytological and urethro-endoscopical follow-up in patients who have undergone a cystoprostatovesciculectomy.
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The authors report 88 cases of ovarian carcinoma containing areas of transitional cell carcinoma (TCC). The tumors were found in women 28-76 years old (mean, 51 years). Fifteen patients presented with stage II, 59 with stage III, and 14 with stage IV disease. Ten neoplasms were composed of only TCC, 48 were predominantly TCC, and 30 had foci of TCC but the predominant component was serous, endometrioid, undifferentiated, or unclassified adenocarcinoma. After the primary resection of the neoplasm, 76 patients received chemotherapy, 4 received chemotherapy and radiotherapy, and 5 received radiotherapy only; 2 refused further treatment and 1 patient died immediately after the first operation. Estimated five-year survival rates were 37% for the entire group and 41% for those who received chemotherapy. Favorable prognostic indicators, statistically significant, were low clinical stage, predominant TCC in the primary tumor, and a negative second-look operation. Other prognostic indicators were the amount of residual tumor after the first operation and tumor differentiation. When the primary neoplasm was predominantly TCC, another prognostic indicator was the type of carcinoma present in the metastases. Five-year follow-up shows that 56% of the patients whose metastases were predominantly TCC have no evidence of disease, whereas only 7% of the patients whose metastases are predominantly non-TCC are disease-free. The authors' study indicates that ovarian carcinomas containing predominant TCC pattern have an excellent response to different chemotherapy regimens. Tumor recurrences and lack of response to chemotherapy are often associated with a change in the histologic appearance of the metastatic lesion.
Seventeen cases of renal small cell carcinoma have been reported in the literature. Approximately half of the reported cases show combined features of transitional cell carcinoma. Presented herein is a case of renal small cell carcinoma in a 37-year-old Japanese male who had been treated for 10 years with famotidine for duodenal ulcer. He suffered from sudden-onset chest pain at presentation and myxoma of the right atrium was suspected. He was treated by atriotomy and a tumor was removed from the right atrium and pulmonary artery. Histological examination, however, revealed it to be small cell carcinoma. Accordingly, a radical operation was performed for the removal of a tumor found in the right kidney. Histological examination of the tumor confirmed the presence of renal small cell carcinoma without any features of transitional cell carcinoma. It is reported that long-term administration of an histamine 2 (H2) receptor antagonist may produce carcinoid tumors in rodents and enterochromaffin-like cell hyperplasia in humans. The possible relationship between neuroendocrine carcinoma and H2 receptor antagonist therapy is discussed.
PURPOSE: Autocrine expression of interleukin (IL)-6 by transitional cell carcinoma (TCC) in response to bacillus Calmette-Guerin (BCG) may have an important role in promoting BCG adherence to TCC and consequently in BCG treatment efficacy. IL-6 expression in response to BCG requires nuclear factor (NF)-kappaB mediated signal transduction. We evaluated the influence of androgens on BCG induced, NF-kappaB mediated IL-6 expression. MATERIALS AND METHODS: Reverse transcriptase-polymerase chain reaction was used to confirm androgen receptor expression in the human TCC lines 253J and T24. A reporter construct containing an androgen response element was used to establish the integrity of androgen mediated signal transduction. Subsequently the dose dependent effect of dihydrotestosterone (DHT) on BCG induced IL-6 expression and NF-kappaB signaling was evaluated. Two pharmacological androgen receptor blockers were used to determine if receptor blockade inhibited the effect of DHT on activation of the androgen response element, NF-kappaB signaling and BCG induced IL-6 expression. RESULTS: The 2 human TCC lines expressed androgen receptor and demonstrated intact androgen stimulated signaling pathways. DHT suppressed BCG induced, NF-kappaB mediated signaling and IL-6 expression in a dose dependent manner. DHT decreased mRNA levels of IL-6, expression of the full-length IL-6 promoter construct and expression of an NF-kappaB specific reporter construct in response to BCG relative to controls. Competitive pharmacological blockade of androgen receptor inhibited the effect of DHT on BCG induced signaling in dose dependent fashion. CONCLUSIONS: DHT down-regulates NF-kappaB mediated IL-6 expression by human TCC lines in response to BCG. This effect depends on a functional androgen receptor signaling pathway and it can be blocked by the inhibition of androgen/androgen receptor binding.
PURPOSE: We tested the discrimination ability of 2 monoclonal antibodies, mAB 90 and 2-2, in renal carcinomas, including renal cell carcinoma and transitional cell carcinoma of the kidney. MATERIALS AND METHODS: Two monoclonal antibodies raised in renal adenocarcinoma (mAB 90, IgG3 subclass and mAB 2-2, IgG1 subclass), have been generated in our laboratory by hybridoma technique. The tumor associated antigens recognized by these IgG subclass monoclonal antibodies are located in the cell membrane of tumor cells. Antibodies were purified from mice ascites through protein A-Sepharose 4B affinity column and then conjugated with fluorescein isothiocyanate fluorescence by dimethyl sulfoxide method. The binding activity of these antibodies was measured by direct immunofluorescence method and analyzed in a flow cytometer. Forty-five cases of renal cell carcinoma and 16 cases of transitional cell carcinoma of the renal pelvis were collected, and the recognition power of these 2 antibodies was tested. Frozen tumor tissues were prepared and allocated into single cell suspensions in phosphate buffered saline before adding diluted (1:10) conjugated antibodies. Irrelevant antibody and negative tumor cell lines without any reaction with these antibodies were used as background fluorescence control. RESULTS: Reactivities of mAB 90 and mAB 2-2 for renal cell carcinoma tissues were 80 and 91%, respectively. On the contrary the reactivities of mAB 90 and mAB 2-2 for transitional cell carcinoma of renal pelvis tissues were 0 and 69%, respectively. mAB 90 (+)/mAB 2-2 (-) expression pattern had 76% accurate diagnostic rate for renal cell carcinoma and mAB 90 (+)/mAB 2-2 (+) pattern had 69% accurate diagnostic rate for transitional cell carcinoma of the kidney. CONCLUSIONS: When facing pathologically ambiguous kidney tumors, the binding specificity of mAB 90 and mAB 2-2 may be useful for discrimination between renal cell carcinoma tumors and transitional cell carcinoma of the renal pelvis.
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Nested variants of transitional cell carcinomas (TCC-NVs) are relatively rare neoplasms in the urinary bladder, but at least 25 cases have been described. This disease is characterized by the pathological finding of irregular nests and/or tubules of transitional carcinoma cells infiltrating the lamina propria without involvement of the mucosal layer. In our case, diagnosed by open biopsy, there were scattered tumor cells observed from the muscle layer to the subserosa, with a tendency toward increasing cellular anaplasia with the depth of invasion. Since the prognosis of TCC-NV is generally poor, comprehensive chemotherapy was performed. No changes were observed on computed tomography and the performance status (0) remained the same after 1 year, so the treatment was considered effective. We conclude that open biopsy should be carried out without hesitation when bladder cancer is suspected, even if there are negative findings of repeated urinary cytology examination and/or endoscopic cold cup biopsy. Immunohistochemical analysis may help in the diagnosis of TCC-NVs derived from epithelial cells. Diagnosis and treatment at an early stage should reduce the mortality of patients with TCC-NVs.
Herein we report a rare combination of two urological tumors simultaneously: renal cell carcinoma of the kidney and transitional cell carcinoma of the bladder. A 67 year old male presented with hematuria. He was diagnosed with left renal cell carcinoma and transitional cell carcinoma of the bladder. Subsequently this patient underwent left nephrectomy (palliative) to control the pain and transurethral resection of bladder tumor. The clinical picture, radiographic and histological finding are presented, as well as the treatment offered.
From 1983 to 1986, 63 male patients received various regimens of intravesical therapy for superficial transitional cell carcinoma of the bladder. Of these 63 patients 10 were subsequently diagnosed as having transitional cell carcinoma of the prostate. Five of the 10 patients had no tumor remaining in the bladder at diagnosis of transitional cell carcinoma of the prostate. In 3 patients tumor in the prostate was more invasive than tumor in the bladder. In 2 patients tumor involvement was greater in the bladder than in the prostate. Patients undergoing treatment with intravesical therapy for transitional cell carcinoma of the bladder, especially those receiving multiple courses for prolonged periods, should be monitored closely for the development of transitional cell carcinoma of the prostate.
Prostatic adenocarcinoma and urothelial carcinoma (transitional cell carcinoma) may coexist in the prostate. However, a carcinoma with mixed features has not been recognized. Four cases, three surgical pathology cases and one autopsy case of prostatic adenocarcinoma with urothelial carcinoma features, were retrospectively found in a urological pathology teaching file maintained from 1984 to 1993. Subsequently, 181 consecutive cases of radical prostatectomy from 1994 to 1999 were reviewed, and two prostatic adenocarcinoma areas with features of urothelial carcinoma were identified. Areas with urothelial carcinoma features were identified in the intraductal component of the carcinoma in five cases and in the invasive component in three cases. The intraductal carcinoma with urothelial carcinoma areas usually merged with regions of prostatic adenocarcinoma with a papillary or cribriform pattern. All prostatic adenocarcinomas having areas with urothelial carcinoma features were of high stage, and five of six cases had ductal features. The urothelial carcinoma component displayed a positive reactivity for thrombomodulin and negative or weaker reactivity for PAP and PSA than the prostatic adenocarcinoma component in the same tumor. Excluding the case noted at autopsy, all patients died of the disease within 3 years. Urothelial carcinoma features were usually associated with ductal carcinoma of high stage. Areas of prostatic adenocarcinoma with urothelial carcinoma features should be considered histopathologically as areas of mixed carcinoma of the prostate. Prostatic adenocarcinoma with areas of urothelial carcinoma features may pose a difficult differential diagnosis problem with urothelial carcinoma, especially with small biopsies with focal weak immunoreactivity for PAP, PSA, and thrombomodulin.