Amyloidosis is a heterogeneous group of disorders and may be classified as systemic or localized on the basis of the distribution of amyloid deposition. Infrequently, the urinary tract and supporting retroperitoneum may be involved, and the imaging findings are nonspecific and diverse. Localized amyloidosis usually involves the bladder and often mimics malignancy. Less frequently, the ureter, renal pelvis, and urethra are involved. The most common findings of amyloid deposition are focal or diffuse wall thickening in the urinary tract with intramural calcification that often results in ureteral obstruction. When the renal parenchyma is involved, patients generally develop nephrotic-range proteinuria, and the kidneys appear atrophic with cortical thinning. In systemic amyloidosis, amyloid may infiltrate the retroperitoneal and pelvic soft tissues, encasing the urinary tract, with diffuse soft-tissue thickening and slowly progressive calcification. In both localized and systemic amyloidosis, amyloid lesions are characteristically hypointense at T2-weighted magnetic resonance imaging. Because myeloma or lymphoma is often present with systemic amyloidosis, biopsy is necessary to diagnose the condition. Amyloid lymphadenopathy characteristically appears as nodal enlargement with calcification and low attenuation at computed tomography. Radiologists should be familiar with the imaging features of amyloidosis that, in the appropriate clinical context, may indicate the diagnosis.
Purpose: Clear cell renal carcinoma (ccRCC) is strongly associated with loss of the von Hippel-Lindau (VHL) tumor suppressor gene. The VHL gene is functionally lost through hypermethylation in up to 19% of sporadic ccRCC cases. We theorized that re-expressing VHL silenced by methylation in ccRCC cells, using a hypo-methylating agent, may be an approach to treatment in patients with this type of cancer. We test the ability of two hypo-methylating agents to re-express VHL in cell culture and in mice bearing human ccRCC and evaluate the effects of re-expressed VHL in these models.Experimental Design: Real-time reverse transcription-PCR was used to evaluate the ability of zebularine and 5-aza-2-deoxycytidine (5-aza-dCyd) to re-express VHL in four ccRCC cell lines with documented VHL gene silencing through hypermethylation. We evaluated if the VHL reexpressed after hypo-methylating agent treatment could recreate similar phenotypic changes in ccRCC cells observed when the VHL gene is re-expressed via transfection in cell culture and in a xenograft mouse model. Finally we evaluate global gene expression changes occurring in our cells, using microarray analysis.Results: 5-Aza-dCyd was able to re-express VHL in our cell lines both in culture and in xenografted murine tumors.Well described phenotypic changes of VHL expression including decreased invasiveness into Matrigel, and decreased vascular endothelial growth factor and glucose transporter-1 expression were observed in the treated lines. VHL methylated ccRCC xenografted tumors were significantly reduced in size in mice treated with 5-aza-dCyd. Mice bearing nonmethylated but VHL-mutated tumors showed no tumor shrinkage with 5-aza-dCyd treatment.Conclusion: Hypo-methylating agents may be useful in the treatment of patients having ccRCC tumors consisting of cells with methylated VHL.
Most solid epididymal masses (94%) are benign. A size of greater than 1.5 cm and the presence of color Doppler flow may help identify possible malignant masses.
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