Objective: The aim of the present study was to determine the prognostic significances of markers of preoperative systemic inflammatory response (SIR) in patients with ovarian clear cell carcinoma (OCCC).

Background: Silibinin, a natural polyphenolic flavonoid, has been reported to induce cell death in various cancer cell types. However, the molecular mechanism is not clearly defined. Our previous study showed that silibinin induces glioma cell death and its effect was effectively prevented by calpain inhibitor. The present study was therefore undertaken to examine the role of calpain in the silibinin-induced glioma cell death.Methods: U87MG cells were grown on well tissue culture plates and cell viability was measured by MTT assay. ROS generation and △ψ_mwere estimated using the fluorescence dyes. PKC activation and Bax expression were measured by Western blot analysis. AIF nuclear translocation was determined by Western blot and immunocytochemistry.Results: Silibinin induced activation of calpain, which was blocked by EGTA and the calpain inhibitor Z-Leu-Leu-CHO. Silibinin caused ROS generation and its effect was inhibited by calpain inhibitor, the general PKC inhibitor GF 109203X, the specific PKC_δinhibitor rottlerin, and catalase. Silibinin-induce cell death was blocked by calpain inhibitor and PKC inhibitors. Silibinin-induced PKC_δactivation and disruption of △ψ_mwere prevented by the calpain inhibitor. Silibinin induced AIF nuclear translocation and its effect was prevented by calpain inhibitor. Transfection of vector expressing microRNA of AIF prevented the silibinin-induced cell death.Conclusions: Silibinin induces apoptotic cell death through a calpain-dependent mechanism involving PKC, ROS, and AIF nuclear translocation in U87MG human glioma cells.

Shin KH, et al. Ann Lab Med. 2020 Jan;40(1):40-47. https://doi.org/10.3343/alm.2020.40.1.40

Perivascular epithelioid cell tumor (PEComa) is a rare subtype of mesenchymal origin tumor composed of epithelioid cells which exhibits immunohistochemical co-expressions of melanocytic markers and smooth muscle markers. In the first case, malignant uterine PEComa with vaginal and multiple lung metastasis was misdiagnosed preoperatively as uterine leiomyosarcoma despite a preoperative punch biopsy and immunohistochemical analysis of the metastatic vaginal mass. In the second case, synchronous uterine PEComa showing benign histology with lymph node involvement was incidentally detected after a staging operation for ovarian cancer. Definitive diagnosis of uterine PEComa was achieved only after hysterectomy despite preoperative assessment with pelvic magnetic resonance imaging and punch biopsy of metastatic lesion. The authors report two rare cases of uterine PEComa diagnosed postoperatively based on the morphologic and immunohistochemical features.