BackgroundSmall cell neuroendocrine carcinoma (SCNEC) of the ureter is a rare tumour, accounting for less than 0.5% of all ureteral tumours. SCNEC tumours are highly aggressive and patients have a poor prognosis. Ureteral SCNEC colliding with other pathological types of tumours is extremely rare. In this paper, we present the case of a patient with ureteral small cell carcinoma colliding with squamous cell carcinoma and review the literature regarding the clinicopathological features, treatment and prognosis of thus tumour. To the best of our knowledge, this is the second identified case of ureteral SCNEC colliding with SCC.Case PresentationA 64-year-old male patient presented with a history of 1 month of gross haematuria and 3 months of left flank pain. CT urography revealed a soft tissue mass in the upper ureter, which was slightly enhanced on contrast-enhanced CT. Nephroureterectomy was performed after the patient was diagnosed with a tumour in the left ureter. Microscopy and immunohistochemical examination confirmed the mass to be a SCNEC collision with SCC. Two months after the surgery, the patient received adjuvant chemotherapy (cisplatin/etoposide). After 14 months of follow-up, no local recurrence or distant metastasis was found.ConclusionUreteral collision carcinoma with SCNEC predominantly occurs in Asian individuals, is difficult to diagnose preoperatively and is highly invasive. The current management of ureteral collision carcinoma is a comprehensive treatment based on surgery.
Highlights
The bladder cavernous hemangioma (BCH) is a benign non-urothelial tumor rarely occurred in the urinary bladder.
Treatment options are vary for individuals and most are with favorable follow-ups.
A history of cancer related radiation therapy seems to be a risk factor for BCH.
It is important to differentiate them from malignant neoplasms since they have extremely different prognostic features and therapeutic strategies.
Nondegradable transvaginal polypropylene meshes for treating pelvic organ prolapse (POP) are now generally unavailable or banned due to serious adverse events. New tissue engineering approaches combine degradable scaffolds with mesenchymal stem/stromal cells from human endometrium (eMSC). In this study, we investigate effect of microRNA-138 (miR-138) regulation on bone marrow-derived mesenchymal stem cells (BMSCs) and the efficacy of BMSC transplantation therapy in a rat POP model. We first identified FBLN5 as a target of miR-138. miR-138, fibulin-5 (FBLN5), interleukin-1β (IL-1β), and elastin expression in uterosacral ligament of POP patients and controls were detected by reverse transcription quantitative polymerase chain reaction (RT-qPCR) and western blot analysis. After isolation and identification, BMSCs were treated to alter their expression of miR-138 or FBLN5. Proliferation of BMSCs was analyzed by CCK-8. After establishing the rat pelvic floor dysfunction (PFD) model, we evaluated efficacy of BMSC injection by applying leak point pressure (LPP) and the conscious cystometry (CMG) tests. miR-138 inhibition resulted in increased viability of BMSCs and elevated their secretion of elastin, while downregulating IL-1β expression. BMSCs with inhibited miR-138 improved LPP and conscious CMG results
in vivo
. Taken together, miR-138 could be a potential therapeutic target for treating POP in conjunction with tissue engineering.
Background: To investigate the expression of Interleukin-6, Interleukin-6 in prostate cancer tissues and its effect on migration and evasiveness of cancer cells. Material and Methods: The releasing of Interleukin-6, Tumor necrosis factor-α in prostate cancer
cells was detected by ELISA method. For prostate cancer cells after knockout, additional Interleukin-6 or Tumor necrosis factor-α induction was given in vitro. After 12 h of culture, the effects of Interleukin-6, Tumor necrosis factor-α on the migration and
evasiveness of prostate cancer cells were observed by Western blot method and matrices invasion experiment. Results: The expression of epithelial mesenchymal transition-related proteins, the migration and invasion ability of prostate cancer cells in each gene knockout group were significantly
reduced. After induction of inflammatory factors (Interleukin-6 or Tumor necrosis factor-α) in the gene knockout group for 12 h, the expression levels of epithelial mesenchymal transition-related proteins, the migration and aggressiveness of prostate cancer were significantly
higher than those after knockout. Conclusion: Interleukin-6 and Tumor necrosis factor-α can induce epithelial mesenchymal transition in LNCaP and PC3 cells, promote cell invasion and metastasis, and provide a new direction for future research.
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