[Strategy of reoperation for pheochromocytoma and paraganglioma].

OBJECTIVE: To explore the surgical strategy and experience of reoperation for pheochromocytoma and paraganglioma which is very challenging. METHODS: The clinical data of 7 patients with pheochromocytoma and paraganglioma who underwent reoperation in Department of Urology, Peking University Third Hospital from August 2016 to February 2021 were analyzed retrospectively. There were 4 males and 3 females, with an average age of (44.1±11.5) years (28-60 years), 6 cases on the right side and 1 case on the left side. The causes of the operations included: (1) 2 cases of tumor recurrence after resection; (2) The primary operations failed to completely remove the tumors in 3 cases, because the tumors were large and closely related to blood vessels. (3) Pheochromocytoma and paraganglioma wasn't diagnosed before primary operation, therefore, drug preparation wasn't prepared. Two cases were interrupted by severe blood pressure fluctuations during the primary operations. Imaging evaluation, catecholamine biochemical examination and adequate adrenergic α receptor blockers were administrated in all the cases. The surgical approaches included open transperitoneal surgery in 4 cases, robot-assisted laparoscopy in 1 case and retroperitoneal laparoscopy in 2 cases. The innovative techniques included mobilization of the liver, inferior vena cava transection and anastomosis, and transection of left renal vein. RESULTS: The average tumor size was (8.0±3.2) cm (3.6-13.9 cm). The median interval between the reoperation and the primary operation was 9 months (IQR: 6, 19 months). The median operation time was 407 min (IQR: 114, 430 min) and the median blood loss was 1 500 mL (IQR: 20, 3 800 mL). Operations of 5 cases were performed successfully, and 1 case failed only by exploration during the operation. One case died perioperatively. There were 5 cases of intraoperative blood transfusion, the median transfusion volume of red blood cells was 800 mL (IQR: 0, 2 000 mL). One case experienced postoperative lymphorrhagia, and recovered after conservative treatment. The renal function was normal in 2 cases after resection and anastomosis of inferior vena cava or transection of left renal vein. The average postoperative hospital stay was (7.2±3.3) d (4-13 d). The median follow-up time of 6 patients was 33.5 months (IQR: 4.8, 48.0 months). The case who failed in the reoperation still survived with tumor and there was no recurrence in the rest of the patients. CONCLUSION: The reoperation of pheochromocytoma and paraganglioma, which can not be resected in the primary operation or recurred postoperatively, is difficult with high risk of hemorrhage, and there is a risk of failure and perioperative death. Different surgical approaches and strategies need to be adopted based on the different situation.

Downregulation of long non-coding RNA DUXAP10 inhibits proliferation, migration, and invasion of renal cell carcinoma.

OBJECTIVE: Renal cell carcinoma (RCC) is the most common kidney malignancy that frequently leads to metastasis. Increasing evidence has shown that long non-coding RNAs (lncRNAs) play crucial roles affecting the progression of RCC. The role of lncRNA DUXAP10 in the evolution of RCC has not been defined yet. This project was designed to clarify the effects of DUXAP10 on the proliferation and tumorigenesis of RCC. PATIENTS AND METHODS: We examined the expression of DUXAP10 in the Cancer Genome Atlas (TCGA) and ONCOMINE oncology databases. Then, we performed quantitative reverse-transcription polymerase chain reaction (qRT-PCR) to evaluate DUXAP10 expression in human RCC tissues and cell lines. The correlation between the expression of DUXAP10 and clinical characteristics of RCC patients was analyzed by univariate and Kaplan-Meier analyses. To unveil the biological function of DUXAP10 in cell cycle progression, cell growth, and invasion of RCC, we conducted knockdown experiments in vitro. qRT- PCR and western blotting assays were performed to further investigate the function of DUXAP10 in cancer biology. RESULTS: The data from TCGA showed that the expression of DUXAP10 was upregulated in tissues of RCC compared with normal tissues. Moreover, ONCOMINE database analysis indicated that high DUXAP10 levels were correlated with high clinical stages, inferior TNM classification, and poor overall survival. Furthermore, the results indicated that knockdown of DUXAP10 remarkably inhibited the RCC cell growth, mobility, and invasion, in association with the upregulation of E-cadherin and downregulation of cyclin D, cyclin E, CDK4, N-cadherin, and vimentin. CONCLUSIONS: Our findings highlight the oncogenic role of DUXAP10 in RCC and that DUXAP10 may serve as a novel predictive biomarker and therapeutic target for RCC.

Long non-coding RNA DUXAP10 promotes the proliferation, migration, and inhibits apoptosis of prostate cancer cells.

OBJECTIVE: Long non-coding RNA DUXAP10 plays a significant role in the tumorigenesis and development of human cancer. The present study was performed to investigate the role of DUXAP10 in biological functions and underlying molecular mechanisms of prostate cancer cells. MATERIALS AND METHODS: First, the quantitative reverse transcription-polymerase chain reaction (qRT-PCR) was used to detect the expression of DUXAP10 in human prostate cancer cell lines 22RV1, PC3, and DU145. Subsequently, small interfering RNAs (siRNAs) targeting at DUXAP10 mRNA were used to downregulate DUXAP10 expression. Then, the biological functions of DUXAP10 in prostate cancer cells, proliferation, migration, and apoptosis were studied by the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, colony-formation assay, cell cycle analysis, transwell migration assay, wound healing assay, and cell apoptosis assay, respectively. Finally, qRT-PCR analysis and Western blot assay were used to investigate the molecular mechanisms of DUXAP10 underlying the progression of prostate cancer. RESULTS: Results showed that the expression of DUXAP10 was higher in PC3 and DU145 cell lines than that in the 22RV1 cell line. Additionally, the knockdown of DUXAP10 could remarkably inhibit the proliferation, migration, and induce apoptosis of prostate cancer cells, and significantly increase the number of G0/G1 cells in PC3 and DU145 cell lines. Moreover, DUXAP10 could promote the development of prostate cancer by regulating the process of epithelial-mesenchymal transition (EMT). CONCLUSIONS: The findings of this study suggested that the down-regulation of DUXAP10 expression suppressed the progression of prostate cancer by inhibiting cell proliferation, migration and promote cell apoptosis.