Primary renal neuroendocrine tumors (NETs) are extremely rare among renal malignancies. According to pathological manifestations, carcinoid can be divided into four types: typical carcinoid, atypical carcinoid, large cell and small cell neuroendocrine carcinoma. Primary or secondary retroperitoneal carcinoid is even rarer than renal carcinoid. This article reports a patient with renal carcinoid complicated with retroperitoneal metastasis, who developed retroperitoneal metastasis 15 years after radical nephrectomy. Through the analysis of this case and the combination of the existing published literature, it is aimed to provide valuable references for clinicians in treating patients with renal carcinoid or with metastasis.
Increasing evidence suggests that microRNAs (miRNAs) play critical roles in bladder tumorigenesis and development by combining with the 3' untranslated regions (3'-UTRs) of the corresponding mRNAs to negatively regulate gene expression. The role of miR-182-5p in bladder cancer (BC) remains unclear. Therefore, this study aimed to clarify the functional role of miR-182-5p in BC. We predicted candidate mRNAs for miR-182-5p via three databases (TarBase, ENCORI, and miRDB). Dual-luciferase reporter assays and target prediction confirmed FOXF2 as a potential target of miR-182-5p. Quantitative RT-PCR (qRT-PCR) showed that endogenous miR-182-5p expression was significantly upregulated in BC cell lines and clinical samples of BC patients. IHC, western blotting, and qRT-PCR assays indicated that FOXF2 expression was concurrently downregulated in BC tissues and BC cell lines. Gain- and loss-of-function studies showed that the overexpression of miR-182-5p enhanced the proliferation and migration of BC cells, while the downregulation of miR-182-5p showed the opposite results. The effects induced by miR-182-5p were attenuated with the restoration of FOXF2 expression. In BC cells, the upregulation of miR-182-5p not only decreased FOXF2 expression but also markedly increased Sonic hedgehog (SHH) pathway levels. These findings suggested that FOXF2 directly binds to miR-182-5p and that miR-182-5p acts as a tumor promoter in BC genesis and metastasis by targeting FOXF2. In addition, miR-182-5p plays a pro-cancer role by downregulating FOXF2 and activating the SHH pathway.
Ewing sarcoma (ES) or primitive neuroectodermal tumors (PNET) represents a spectrum of poorly differentiated and aggressive malignancies. It rarely arises from the kidney and accounts for less than 1% of renal mass. Given the uncharacteristic clinical symptoms and imaging features, renal Ewing sarcoma (RES) is often diagnosed by postoperative pathology.Herein, we depicted a case of RES, which was administrated in our institution by chief complaints of intermittent left plank pain and palpable abdominal mass. We demonstrated the aggressive behavior of this renal malignancy and summarized its therapeutic modalities and outcomes.The diagnosis of RES relies on integrated analysis including histomorphology, immunohistochemical staining and confirmation of molecular-genetic testing. Despite the surgery and adjuvant therapy, optimized and potent therapeutic regimes are still urgently needed to improve the poor prognosis of RES.
AIM: To observe the curative effect of 4-HPR on bladder tumor using bladder tumor model induced by MNU in SD rats.METHODS: 70 SD rats was randomly divided into 5 groups: control group(Group A),module group(Group B),mould processing group(Group C,Group D,Group E).The bladder perfusion of treatment group was instilled 4-HPR,ADM and BCG respectively.A week after administration,the SD rats were put to death.The immunohistochemistry was used to detecte the expression of COX-2 and MVD,and the TUNEL technique was applied to examine apoptosis.RESULTS:The results of pathological specimens indicated that the 4-HPR,ADM and BCG inducing tumor had an obvious intervention effect(P0.05);Besides,the 4-HPR could inhibit the expression of COX-2,the generation of capillaries,and the spur of apoptosis tumor cells(P0.05).CONCLUSION: The 4-HPR,ADM and BCG to MNU had an intervention effect in carcinogenic process.The 4-HPR had no significant differences in anticancer effect compared with other groups,but had less side effect than the other groups.
Objective:To explore the expression of CD44s and CD44v10 in bladder transitional cell carcinoma(BTCC) and the biological behavior of BTCC. Methods: The expression levels of CD44s and CD44v10 were detected in 60 cases with BTCC and in 6 of normal bladder by immunohistochemical method. Results: The expression level of CD44s was significantly different between BTCC group and control group(P0.001) and the difference was also found in cases of relapse and primary development(P0.001). Conclusion: CD44s and CD44v10 are involved in the progression of BTCC and combined detection of CD44s and CD44v10 may contribute to the early diagnosis of the disease.
Bufalin has been demonstrated to possess a wide range of pharmacological effects. Among these is its antitumour effect, which has been confirmed in multiple organs or tissues and provoked many concerns. However, its cytostatic effect and underlying mechanism in bladder cancer has not thoroughly been elucidated. This study aimed to investigate the hypothesis that Bufalin induces cell apoptosis and inhibits cell growth in bladder cancer through the inactivation of Na+/K+-ATPase (NKA). In the current study, it was demonstrated that Bufalin remarkably inhibited cell viability and induced cell apoptosis in bladder cancer cell line T24. Subsequently, we found that the expression of NKA was significantly supressed in Bufalin-treated cells and the NKA-α3 isoform was most sensitive to Bufalin among all α subunits of NKA. By transfection with NKA-α3 overexpressing plasmids, the expression of the NKA-α3 subunit was upregulated and NKA-α3 overexpression was found to markedly attenuated Bufalin-induced cell apoptosis in T24 cells, suggesting NKA-α3 played a critical role in Bufalin-induced cell apoptosis. Taken together, the present study confirmed that Bufalin promotes tumour apoptosis and inhibits tumour growth in bladder cancer in vitro, and this antitumour effect may be ascribed to the inactivation of NKA.
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