Non-functional paraganglioma of the urinary bladder: a case report

<p>Abstract</p> <p>Introduction</p> <p>Paragangliomas that originate from the urinary bladder are extremely rare. In most series, bladder paragangliomas often cause micturitional attacks. Treatment modalities include transurethral resection and cystectomy (partial or total). Prognosis of bladder paraganglioma is similar to that of adrenal pheochromocytoma.</p> <p>Case presentation</p> <p>A 55-year-old Chinese woman presenting with the sole complaint of lower abdominal pain for one month was admitted to our hospital. Ultrasound and computed tomography revealed a mass on the dome of the bladder measuring 4.0 × 3.0 cm. The tumor was completed removed by laparoscopic partial cystectomy. Histological examination of the tumor indicated paraganglioma of the urinary bladder. The clinical features, diagnosis, management and pathological findings of paraganglioma of the urinary bladder are discussed.</p> <p>Conclusions</p> <p>Bladder paraganglioma should be considered as a differential diagnosis to neoplasm in the urinary bladder, although there is no characteristic symptom. Laparoscopic partial cystectomy may be the first choice in treating paraganglioma of the urinary bladder, offering several advantages such as less invasion, rapid recovery and early discharge from the hospital.</p

Effects of alpha fetoprotein on escape of Bel 7402 cells from attack of lymphocytes

BACKGROUND: Involvement of AFP against apoptosis of tumor cell has been implicated in its evasion of immune surveillance. However, the molecular events of immune escape mechanisms are still unknown. The major observations reported here relate to a possible mechanism by which heptoloma Bel 7402 cells escape immune surveillance in vitro. METHODS: Western blotting and a well-characterized cofocal scanning image were performed to analyze the expression of Fas/FasL and caspase-3 in co-cultured Bel 7402 and Jurkat cells. RESULTS: After co-culture with Jurkat cells, up-regulated Fas and reduced FasL expression could be observed. Treatment with AFP could remarkably inhibit the elevated Fas and, whereas, induce the FasL expression in co-cultured Bel 7402 cells. Cells co-culture could induce the expression of caspase-3 in both cells line. The elevated caspase-3 in Bel 7402 cells was abolished following the treatment of AFP. The expression of caspase-3 was elevated in co-cultured Jurkat cells treated with AFP. No detectable change on the expression of survivin was examined in both cells line. Monoclonal antibody against AFP treatment alone did not obviously influence the growth of cells, as well as the expression of Fas/FasL and caspase-3. However, the effect of AFP could be blocked by antibody. CONCLUSIONS: our results provide evidence that AFP could promote the escape of liver cancer cells from immune surveillance through blocking the caspase signal pathway of tumor cells and triggering the Fas/FasL interaction between tumor cells and lymphocytes