Undifferentiated high-grade pleomorphic sarcoma of the common bile duct: A case report and review of literature.

BACKGROUND: Undifferentiated pleomorphic sarcoma (UPS) is a rare malignant mesenchymal tumor with a poor prognosis. It mainly occurs in the extremities, trunk, head and neck, and retroperitoneum regions. Owing to the lack of specific clinical manifestations and imaging features, UPS diagnosis mainly depends on pathological and immunohistochemical examinations for exclusive diagnosis. Here we report an extremely rare case of high-grade UPS in the common bile duct (CBD). There are limited available data on such cases. CASE SUMMARY: A 70-year-old woman was admitted to our department with yellow eyes and urine accompanied by upper abdominal distending pain for 2 wk. Her laboratory data suggested significantly elevated hepatorenal function levels. The imaging data revealed calculous cholecystitis, intrahepatic and extrahepatic bile duct dilation with extrahepatic bile duct calculi, and a space-occupying lesion at the distal CBD. After endoscopic biliary stenting and symptomatic support therapy, CBD exploration and biopsy were performed. The frozen section indicated malignant spindle cell tumor of the CBD mass, and further radical pancreaticoduodenectomy was performed. Finally, the neoplasm was diagnosed as a high-grade UPS combined with the light-microscopic morphology and immunohistochemical results. CONCLUSION: This extremely rare case highlighted the need for increasing physicians' vigilance, reducing the odds of misdiagnosis, and providing appropriate treatment strategies.

Establishing a reference range for thromboelastography maximum amplitude in patients administrating with antiplatelet drugs.

OBJECTIVE: We aimed to establish the reference range of thromboelastograph (TEG) maximum amplitude (MA) in patients taking antiplatelet drugs. METHODS: Between August 2015 and July 2018, a total of 4614 patients administrating with antiplatelet drugs (clopidogrel and aspirin) were retrospectively analyzed in this study. For MAA parameter, we used the 10th and 90th percentiles to establish a reference range. The Spearman correlation was used for the correlation analysis among the inhibition rate of adenosine diphosphate (ADP%) and MAADP , inhibition rate of arachidonic acid (AA%) and MAAA . Then, through receiver operating characteristic (ROC) curve analysis of the best cutoff point, the reference ranges of MAADP and MAAA could be deduced. Consistency evaluation was performed by statistical analysis of ADP% and MAADP , AA% and MAAA pairing for 4459 patients. RESULTS: The reference range of MAA was 8.1-25.8 mm. The reference range of MAADP was 19.8-43.2 mm, and the corresponding sensitivity of two endpoints was 0.796, 0.856 and specificity were 0.897, 0.904, respectively. The reference range of MAAA was 18.9-37.7 mm, and the corresponding sensitivity of two endpoints was 0.819, 0.829 and specificity were 0.922, 0.896, respectively. The inconsistency rate of ADP% and MAADP , and AA% and MAAA was 20.1% (898 cases) and 16.6% (738 cases), respectively. CONCLUSIONS: The reference range of MAADP and MAAA established by us were better in sensitivity and specificity. MAADP and MAAA were more accurate than conventional inhibition rate analysis in guidance of antiplatelet therapy, especially in patients with excessive low MA or high MAA .

[Effects of CTCF on human liver cancer stem cells and cell proliferation].

OBJECTIVE: To explore the effects of CCCTC-binding factor (CTCF) on human liver cancer stem cells (HepG2) and cell proliferation of HepG2 and Nasopharyngeal carcinoma cell line (CNE1). METHODS: The pEGFP-N1/CTCF, CTCF-shRNA and GFP-shRNA plasmids were constructed and transfected into HepG2 and CNE1 cells, and RT-PCR or Western blot were performed to detect the mRNA or protein levels of CTCF. The subpopulation of CD90+ cancer stem cells in HepG2 cells transfected with CTCF-shRNA plasmid or GFP-shRNA plasmid (as transfection control) were assayed by flow cytometry with the wild type HepG2 cells as control. Proliferation of cells transfected with CTCF-overexpression or CTCF-shRNA plasmid was evaluated by MTT assay. RESULTS: The levels of both mRNA and protein of CTCF were increased in pEGFP-N1/CTCF transfected HepG2 and CNE1 cells compared to that in pEGFP-N1 transfected cells (P < 0.05), and decreased in CTCF-shRNA transfected cells compared to that in cells transfected with GFP-shRNA (P < 0.05). The results of flow cytometry demonstrated that, detection rate of CD90+ cells in cells transfected with CTCF-shRNA plasmid [(1.7330 +/- 0.4177)%] was obviously higher than that of wild-type HepG2 cells [(0.5750 +/- 0.0629)%] and cells transfected with GFP-shRNA plasmid [(0.3500 +/- 0.0866)%] (P < 0.05). The results of MTT analysis showed that, alteration of CTCF had no effect on cancer cell proliferation (P > 0.05). CONCLUSION: CTCF inhibits human liver cancer stem cells but no effect on cell proliferation.

Vigilin is overexpressed in hepatocellular carcinoma and is required for HCC cell proliferation and tumor growth.

Vigilin contains multiple KH domains and is an evolutionarily conserved RNA-binding protein from yeast to the human. Its reported roles in human carcinogenesis are controversial in different types of human cancers. To obtain the specific expression profiles of vigilin in human hepatocellular carcinomas (HCCs), we examined vigilin protein levels in normal human liver, liver cirrhosis, adjacent non-tumor liver and HCC tumor tissues as well as in several HCC cell lines. We discovered that vigilin expression increased progressively from the liver cirrhosis tissue to adjacent non-tumor liver tissue and then to HCC tumor cells. Vigilin protein was also overexpressed in all three HCC cell lines examined, HepG2, BEL7402 and SMMC7721, when compared with the vigilin expression level in the L-02 human embryonic hepatocyte cell line. We further investigated the impact of vigilin knockdown on HCC cell proliferation, survival, motility, tumor growth and sensitivity to chemotherapy. We found that knockdown of vigilin in the BEL7402 HCC cells significantly inhibited their proliferation, colony formation and migration, but largely enhanced the cisplatin treatment-induced growth inhibition of these cells in culture. We also found that vigilin knockdown effectively inhibited the growth of BEL7402 cell-derived xenograft tumors in nude mice by decreasing the proliferation and increasing the apoptosis of the BEL7402 HCC cells. Taken together, these results suggest that progressively upregulated vigilin may serve as a molecular risk marker for HCC development, and targeting vigilin may help to inhibit HCC cell growth, survival and migration.

CTCF-mediated reduction of vigilin binding affects the binding of HP1α to the satellite 2 locus.

CCCTC-binding factor (CTCF) has been implicated in numerous aspects of chromosome biology, and vigilin, a multi-KH-domain protein, participates in heterochromatin formation and chromosome segregation. We previously showed that CTCF interacts with vigilin. Here, we show that human vigilin, but not CTCF, colocalizes with HP1α on heterochromatic satellite 2 and ß-satellite repeats. CTCF up-regulates the transcription of satellite 2, while vigilin down-regulates it. Vigilin depletion or CTCF overexpression reduces the binding of HP1α on the satellite 2 locus. Furthermore, overexpression of CTCF resists the loading of vigilin onto the satellite 2 locus. Thus CTCF may regulate vigilin behavior and thus indirectly influence the binding of HP1α to the satellite 2 locus.

[Expression of vascular growth factors in intestinal tissues in colorectal carcinoma patients with schistosomiasis japonica].

OBJECTIVE: To investigate the differences of mRNA quantitation and protein expression of vascular growth factors including platelet-derived endothelial cell growth factor (PD-ECGF) and vascular endothelial growth factor (VEGF) in intestinal tissues in colorectal carcinoma patients with and without schistosomiasis. METHODS: Thirty colorectal carcinoma patients with schistosomiasis and 30 colorectal carcinoma patients without schistosomiasis were included in this study. The mRNA quantitation and protein expression of PD-ECGF and VEGF in the normal tissue, peri-carcinoma tissue as well as carcinoma tissue obtained from surgical specimens were detected by qRT-PCR and Western blot. RESULTS: The mRNA relative quantitations of PD-ECGF in normal tissue, peri-carcinoma tissue and carcinoma tissue in the colorectal carcinoma patients with schistosomiasis were 1.726, 1.766 and 2.729 times to those in the colorectal carcinoma patients without schistosomiasis, respectively. The corresponding ones of VEGF were 2.138, 1.831 and 3.376 times, respectively. The protein expression levels of PD-ECGF and VEGF in normal tissue, peri-carcinoma tissue and carcinoma tissue were higher in the colorectal carcinoma patients with schistosomiasis than in the colorectal carcinoma patients without schistosomiasis. CONCLUSIONS: The expressions of vascular growth factors including PD-ECGF and VEGF are higher in the colorectal carcinoma patients with schistosomiasis than in the colorectal carcinoma patients without schistosomiasis. Therefore, schistosomiasis may be one of the risk factors of colorectal cancer.