A comparison of the clinical features and prognosis of pancreatic head cancer with that of other periampullary cancers.

BACKGROUND/AIMS: Our purpose was to compare the clinical features and prognosis of pancreatic head cancer with that of other periampullary cancers. METHODOLOGY: The medical records of 82 patients (mean age of 61.67±10.52 years) with ductal adenocarcinoma of the head of pancreas and 73 patients (mean age of 60.52±11.72 years) with other periampullary adenocarcinomas, all of whom had received radical surgery, were retrospectively analyzed. RESULTS: There were no significant differences in age and gender between the groups (both, p>0.05). However, there were significant differences in lymph node metastasis, TNM stage, clear surgical margins, tumor size, and neural invasion between the 2 groups (all p<0.05). Patients with pancreatic head adenocarcinoma had significantly higher red blood cell (RBC) count and hemoglobin (Hb), albumin and pre-albumin levels, and higher platelet and white blood cell (WBC) counts than the patients with other periampullary adenocarcinomas (all p<0.05). No differences in carcinoembryonic antigen (CEA) or CA19-9 were noted between the groups. The 1-year survival rates were not different between the groups (p=0.299). CONCLUSIONS: Pancreatic head carcinoma has different clinical manifestations and biological features than other periampullary cancers.

Downregulation of histone demethylase JMJD1C inhibits colorectal cancer metastasis through targeting ATF2.

Colorectal cancer (CRC) is one of the most common malignant gastrointestinal cancers. Metastasis is a major leading of death in patients with CRC and many patients have metastatic disease at diagnosis. However, the underlying molecular mechanisms are still elusive. Here, we showed that JMJD1C was overexpressed in colon cancer tissues compared to normal samples and was positively associated with metastasis and poor prognosis. Silencing JMJD1C strongly inhibits CRC migration and invasion both in vitro and in vivo. Further, we found that knockdown of JMJD1C decreased the protein and mRNA levels of ATF2, mechanistically, and JMJD1C regulated the expression of ATF2 by modulating the H3K9me2 but not H3K9me1 activity. In addition, we further performed some "rescues experiments". We found that overexpression of ATF2 could reverse the abrogated migration and invasion ability by knockdown of JMJD1C in CRC. Our results demonstrated that an increase of JMJD1C was observed in colon cancer and knockdown of JMJD1C regulated CRC metastasis by inactivation of the ATF2 pathway. This novel JMJD1C/ATF2 signaling pathway may be a promising therapeutic target for CRC metastasis.

Entrapment of a chiral cobalt complex within silver: a novel heterogeneous catalyst for asymmetric carboxylation of benzyl bromides with CO2.

A novel way to accommodate heterogeneous catalysis, CO2 fixation and asymmetric synthesis on one catalyst is reported. The [Co]@Ag composite was prepared for the first time and used for asymmetric carboxylation of benzyl bromides with CO2. All the procedures were performed under mild conditions. Moreover, the [Co]@Ag composite has terrific stability and reusability.

A study of mifepristone/IFN-γ-induced apoptosis of human cholangiocarcinoma cell line FRH-0201 in vitro.

OBJECTIVE: To investigate the effects of mifepristone, a progesterone receptor (PR) antagonist, through the proliferation of human cholangiocarcinoma cell line FRH-0201 in vitro and the possible mechanisms involved. METHODS: A two-step addition of poly-HRP anti-mouse immunoglobulin G detection system was used to detect the expression of PR in FRH-0201 cells. After treatments with various concentrations of mifepristone (10, 20, 40, 80, 160, and 320 µmol/L) at various time intervals (24, 48, and 72 hours), the rate of cell inhibition, the rate of cell apoptosis, and the expression of bax/bcl-2/Fas were analyzed with tetrazolium blue (MTT) assay, flow cytometry, reverse transcription polymerase chain reaction and Western blotting. The effect of mifepristone and mifepristone combined with interferon (IFN)-γ-inducing apoptosis on the cells was observed. RESULTS: Mifepristone remarkably inhibited the proliferation of FRH-0201 cells, which was revealed by MTT assay in a dose- and time-dependent manner. The inhibitory rate gradually increased following the increase of the dosage of mifepristone from a low dosage (10 µmol/L) to a high dosage (320 µmol/L) at different time intervals. Flow cytometry analysis showed mifepristone increased the rate of the FRH-0201 cell-line apoptosis. Notably, the rate of apoptosis increased markedly when the cells were pretreated with IFN-γ and then treated with mifepristone. In addition, mifepristone obviously upregulated bax and Fas expression and downregulated bcl-2 expression. CONCLUSION: Mifepristone effectively inhibited the growth of PR-positive human cholangiocarcinoma cell line FRH-0201 in vitro through multiple mechanisms. Mifepristone combined with IFN-γ might therefore induce the apoptosis of the cell line, which is possibly a beneficial clinical scheme for patients suffering from cholangiocarcinoma.