HLA-G was expressed in a significant number of primary ovarian carcinoma tissues, and HLA-G expression in OVCAR-3 could directly inhibit NK-92 cell lysis. Taken together, our results indicated that expression of HLA-G plays an important role in evasion of ovarian cancer cells from host immunosurveillance.

The mitotic spindle checkpoint (SAC) genes have been considered targets of anticancer therapies. Here, we sought to identify the attractive mitotic spindle checkpoint genes appropriate for human hepatocellular carcinoma (HCC) therapies. Through expression profile analysis of 137 selected mitotic spindle checkpoint genes in the publicly available microarray datasets, we showed that 13 genes were dramatically up-regulated in HCC tissues compared to normal livers and adjacent non-tumor tissues. A role of the 13 genes in proliferation was evaluated by knocking them down via small interfering RNA (siRNA) in HCC cells. As a result, several mitotic spindle checkpoint genes were required for maintaining the proliferation of HCC cells, demonstrated by cell viability assay and soft agar colony formation assay. Then we established sorafenib-resistant sublines of HCC cell lines Huh7 and HepG2. Intriguingly, increased TTK expression was significantly associated with acquired sorafenib-resistance in Huh7, HepG2 cells. More importantly, TTK was observably up-regulated in 46 (86.8%) of 53 HCC specimens. A series of in vitro and in vivo functional experiment assays showed that TTK overexpression promoted cell proliferation, anchor-dependent colony formation and resistance to sorafenib of HCC cells; TTK knockdown restrained cell growth, soft agar colony formation and resistance to sorafenib of HCC cells. Collectively, TTK plays an important role in proliferation and sorafenib resistance and could act as a potential therapeutic target for human hepatocellular carcinoma.

No abstract

Metaplastic thymoma is an extremely rare tumor. To date, only 17 cases of metaplastic thymoma have been reported. To the best of the authors' knowledge, this is the second reported case of a sarcomatoid carcinoma arising in metaplastic thymoma; the carcinoma in this case is larger than that in the previous case. A 63-year-old woman with cough and asthenia for 2 weeks was admitted to the hospital. Computed tomography (CT) revealed a giant mass on the right side of the front mediastinum medium. The mediastinal tumor was excised, and additional pathological examinations, immunohistochemical tests, and electron-microscopic tests were performed. The tumor was diagnosed as a sarcomatoid carcinoma arising in metaplastic thymoma. Here, the authors discuss the clinical pathology of the sarcomatoid carcinoma arising in metaplastic thymoma and describe the biological behaviors with respect to the pathological features.

Methyl CpG binding protein 2 (MeCP2) is a methylated DNA binding protein. MeCP2 located on the X chromosome plays key roles on neurological disorders, especially on Rett syndrome. 1,2 Recently, it has been confirmed that MeCP2 mutations could cause intellectual disability. 3 Methyl CpG binding protein 2 was identified as a member of intrinsically disordered proteins (IDPs), which have rarely structured elements. 4 In fact, only 40% of the protein structure of MeCP2 could form the classical tertiary structure, such as α-helices, β-sheets, and