Meigs' syndrome caused by granulosa cell tumor accompanied with intrathoracic lesions: A case report.

BACKGROUND: Meigs' syndrome is regarded as a benign ovarian tumor accompanied by pleural effusion and ascites, both of which resolve after removal of the tumor. Patients often seek treatment in the Department of Respiratory and Critical Care Medicine or other internal medicine departments due to symptoms caused by ascites or hydrothorax. Here, we report a rare case of Meigs' syndrome caused by granulosa cell tumor accompanied with intrathoracic lesions. CASE SUMMARY: A 52-year-old women was admitted to the Department of Respiratory and Critical Care Medicine due to coughing and expectoration accompanied with shortness of breath. Chest X-ray and chest computed tomography showed a modest volume of pleural fluid with pleural thickening in the right lung. The carbohydrate antigen 125 (CA125) concentration was 150.8 U/mL (normal, 0-35 U/mL) and no tumor cells were observed in pleural fluid. Nodules and a neoplasm with a fish meat-like appearance in the parietal pleura and nodules with a 'string of beads'-like appearance in the diaphragm were found by thoracoscopic examination. Furthermore, pelvic magnetic resonance revealed a pelvic mass measuring about 11.6 cm × 10.0 cm × 12.4 cm with heterogeneous signal intensity and multiple hypointense separations. Total abdominal hysterectomy, bilateral adnexectomy, and separation of pelvic adhesion were performed under general anesthesia. The pathology results showed granulosa cell tumor. At the 2-mo follow-up after the surgery, the hydrothorax subsided, and the CA125 level returned to normal. CONCLUSION: For postmenopausal women with unexplained hydrothorax and elevated CA125, in addition to being suspected of having gynecological malignancy, Meigs' syndrome should be considered.

Karyopherin α2 induces apoptosis in tongue squamous cell carcinoma CAL-27 cells through the p53 pathway.

Tumor onset and progression are associated with dysfunction of the nuclear transport machinery at the level of import and export receptors. However, the role of Karyopherin α2 (KPNA2) in human tongue squamous cell carcinoma (TSCC) remains unknown. We assessed the proliferation, apoptosis and migration of TSCC CAL-27 cells using wound healing, Transwell and MTT assays, western blotting, electron microscopy and acridine orange/ethidium bromide staining following knockdown of KPNA2. The results revealed the antiproliferative, proapoptotic and anti-migratory effects of KPNA2 silencing on the TSCC CAL-27 cells. Moreover, the knockdown of KPNA2 proved to be accompanied by the upregulation of active caspase-3, cytochrome c, Bax, Bad and decreased expression of Bcl-2, p-Bad and XIAP. KPNA2 activated the caspase-dependent pathway in the CAL-27 cells with upregulation of p53, p21Cip1/Waf1 and p16INK4a. Thus, the present study demonstrated that p53/p21Cip1/Waf1/p16INK4a may be an important pathway involved in the function of KPNA2 in TSCC CAL-27 cells.