Leydig cell tumor of the testis with characteristic contrast patterns of tumor and non-tumorous testicular parenchyma on MRI: a case report.

PURPOSE: Testicular Leydig cell tumor (LCT) is a rare subtype of testicular neoplasms that occurs in the interstitial tissue of testes, accounting for 1-3% of total testicular masses removed annually. We report a case of 70-year-old man diagnosed as testicular LCT. This report demonstrates a testicular LCT with intratumoral and non-tumorous testicular parenchymal enhancement in the affected testis, which should be considered characteristic findings of LCT. METHODS: Ultrasonography showed a hypoechoic mass. On magnetic resonance imaging, the tumor showed low signal intensity comparable to the surrounding testicular tissue on T1-weighted images (T1WI) and low signal intensity on T2-weighted images (T2WI). On gadolinium contrast-enhanced T1WI (CE-T1WI), the tumor showed a rapid and marked wash-in and subsequent prolonged washout. The spared, non-tumorous testicular parenchyma showed slow and progressive enhancement in the early phase, which was as strong as or stronger than that of the mass in the delayed phase. The patient underwent right orchiectomy. RESULTS: Pathologically, the tumor was diagnosed as a testicular Leydig cell tumor (LCT). Leydig cell proliferation was observed with well-developed microvessels, atrophy of the seminiferous tubules, and stromal edema in the non-tumorous testicular parenchyma. Leydig cells in the non-tumorous parenchyma were positive for estrogen receptors. CONCLUSION: Since the contrast findings in the non-tumorous testicular parenchymal region on CE-T1WI likely match the histopathological features of LCT, our case suggests that the presence of non-tumorous testicular parenchymal enhancement on imaging might indicate a diagnosis of LCT.

Killer cell lectin-like receptor G1 binds three members of the classical cadherin family to inhibit NK cell cytotoxicity.

Killer cell lectin-like receptor G1 (KLRG1) is an inhibitory receptor expressed on subsets of natural killer (NK) cells and T cells, for which no endogenous ligands are known. Here, we show that KLRG1 binds three of the classical cadherins (E-, N-, and R-), which are ubiquitously expressed in vertebrates and mediate cell-cell adhesion by homotypic or heterotypic interactions. By expression cloning using the mouse KLRG1 tetramer as a probe, we identified human E-cadherin as a xenogeneic ligand. We also identified a syngeneic interaction between mouse KLRG1 and mouse E-cadherin. Furthermore, we show that KLRG1 binds N- and R-cadherins. Finally, we demonstrate that E-cadherin binding of KLRG1 prevents the lysis of E-cadherin-expressing targets by KLRG1+ NK cells. These results suggest that KLRG1 ligation by E-, N-, or R-cadherins may regulate the cytotoxicity of killer cells to prevent damage to tissues expressing the cadherins.

Interleukin-6-producing thymic squamous cell carcinoma associated with Castleman's disease and nephrotic syndrome.

When a 63-year-old man was hospitalized with nephrotic syndrome due to focal segmental glomerulosclerosis, a mediastinal mass was discovered. A biopsy specimen obtained by mediastinoscopy showed findings compatible with the plasma cell type of Castleman's disease. Fever, anemia, and anti-nuclear antibody were present. Serum concentrations of gamma globulin, acute phase proteins, and, most strikingly, interleukin-6 (IL-6) were elevated. Methylprednisolone pulse therapy resulted in no clinical improvement. Pathologic examination of the resected thymic tumor showed a squamous cell carcinoma immunoreactive for IL-6. To our knowledge, this case represents the first reported IL-6-producing thymic squamous cell carcinoma associated with Castleman's disease and nephrotic syndrome.