Solid pseudopapillary tumors (SPTs) occurring as primary tumors outside the pancreas are exceedingly rare. The present study reports such a case occurring as a non-functional adrenal tumor in a 22-year-old female. The tumor was completely removed from the retroperitoneum by laparoscopic surgery. A well-defined, encapsulated tumor measuring 6×6×5 cm was histologically characterized by a combination of the solid and pseudopapillary growth patterns of tumor cells with eosinophilic cytoplasm. Ectopic pancreatic tissue was also found histologically within the resected tumor. On immunostaining, the tumor was positive for progesterone receptor, CD56, cytokeratin and CD10. The morphological and immunohistochemical features were compatible with those of SPT. To the best of our knowledge, this is the first case report of extrapancreatic SPT with evidence of a pre-existing ectopic pancreas in the retroperitoneum. A review of the published English literature uncovered 12 cases of extrapancreatic SPTs, and revealed that extrapancreatic SPTs are likely to have a favorable clinical course and a clinical profile similar to their pancreatic counterparts.

Objective: Epidemiologic studies investigating the association between dietary carbohydrates as well as glycemic index and glycemic load (markers of carbohydrate quality) and bladder cancer risk have yielded inconsistent results. The aim of the present meta-analysis is to summarize the evidence on this association. Materials and Methods: A comprehensive literature search of articles published by December 2019 was performed in PubMed, Scopus, and Web of Science databases. A random-effects model was used to calculate the pooled odds ratios (ORs) and their corresponding 95% confidence intervals (CIs). Results: Twelve observational studies were included in the final analysis. There was no evidence of an association between consumption of carbohydrates and bladder cancer risk (pooled OR, 1.04; 95% CI, 0.92-1.17). No statistically significant association between glycemic load and bladder cancer was likewise found (pooled OR, 1.10; 95% CI, 0.85-1.42). However, there was a significant positive association between glycemic index and bladder cancer risk (pooled OR, 1.25; 95% CI, 1.11-1.41). In the dose-response analysis, the pooled OR (95% CI) per 10 units of glycemic index per day was 1.02 (95% CI, 1.01-1.04). Conclusion: In this meta-analysis, glycemic index showed a positive linear association with bladder cancer risk.

Prostatic-type polyps are uncommon lesions in the urinary tract. They are sometimes found in the lower urinary tract, particularly on the posterior urethra, but are rarely found in the bladder. We report a case of 15-year-old boy who presented with dysuria. Routine ultrasonography showed a mass in the bladder arising near the internal orifice of urethra. Further inspection with cystoscopy followed by transurethral resection and pathology confirmed the lesion to be a prostatic-type polyp. An overview of other similar case studies showed that the pathogenesis of this condition is controversial, haematuria and dysuria are common clinical symptoms and endoscopic transurethral resection is the best treatment option. Since the polyp is benign, recurrence and progression of this disorder is unlikely to occur.

Emerging evidence has indicated that dysregulation of miR-362-3p is involved in the initiation and progression of several types of human cancers. However, the molecular mechanism of miR-362-3p in renal cell carcinoma (RCC) is still not completely clear. In this study, we found that miR-362-3p was frequently down-regulated in human RCC tissues. Overexpression of miR-362-3p in RCC cells significantly suppressed the proliferation, cell cycle and motility in vitro and in vivo via regulating AKT/FOXO3 signaling. We further confirmed that SP1 was a direct target of miR-362-3p. Knockdown of SP1 expression by a small interfering RNA (siRNA) phenocopied the effect of miR-362-3p overexpression in RCC cells. In conclusion, the current results provide evidence for the role of miR-362-3p in the pathogenesis of RCC and thus miR-362-3p may serve as an attractive candidate for RCC therapy.

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