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This study aimed to evaluate the relationship of fascin-1, matrix metalloproteinase (MMP)-2, MMP-9, cortactin, survivin, and epidermal growth factor receptor (EGFR) expression with clinicopathological parameters for the four most common ovarian surface epithelial carcinomas. Six biomarkers were investigated immunohistochemically using tissue microarrays of 185 specimens including 79 serous cystadenocarcinomas, 47 mucinous cystadenocarcinomas, 45 endometrioid adenocarcinomas, and 14 clear cell carcinomas. The four most common ovarian carcinomas showed significant expression of fascin-1, cortactin, survivin, and EGFR, but not of MMP-2 and MMP-9. In addition, higher immunostaining scores for fascin-1 in mucinous cystadenocarcinomas correlated with T stage, N stage, American Joint Committee on Cancer AJCC clinical stage, and a poorer survival rate; for cortactin in serous cystadenocarcinomas correlated with T stage; for cortactin in clear cell carcinomas correlated with T and clinical AJCC stages; and for survivin in clear cell carcinomas correlated with T stage and AJCC clinical stage. In addition, higher immunostaining scores for fascin-1, cortactin, and survivin correlated with poorer tumor differentiation in serous, mucinous, and endometrioid adenocarcinomas. Thus, the expression of fascin-1, cortactin, and survivin may be helpful in evaluating the aggressiveness of ovarian mucinous, serous, and clear cell adenocarcinoma. Additionally, the expression of fascin-1 may be an independent prognostic risk factor in mucinous cystadenocarcinoma.

Enterogastric reflux (EGR) is regarded as an unavoidable consequence of distal gastrectomy. We evaluated the efficacy of Roux-en-Y (RY) gastrojejunostomy and Braun enteroenterostomy (BEE) for preventing EGR. Between January 2002 and January 2005, 60 patients who underwent distal gastrectomy for gastric cancer or peptic ulcers were divided into RY, Billroth II reconstruction (BII) without or with BEE (BII+B) according to reconstructive method. After 12 months, EGR and mucosal alterations of the remnant stomach were evaluated using biliary scintigraphy, endoscopy, and histology. Scintigraphy showed fasting and postprandial EGR into the remnant stomach occurred in 5.3% and 21.1% of the RY group, 62.1% and 93.1% of the BII group, and 50.0% and 91.7% of the BII+B group, respectively. Endoscopy showed bile reflux occurred in 15.8% of the RY group, 75.9% of the BII group, and 83.3% of the BII+B group. In addition, the prevalence of Helicobacter pylori (HP) infection in the RY group was less than in the other groups (P<0.02). Therefore, RY after distal gastrectomy was effective in reducing EGR and HP infection. BEE was ineffective in diverting bile flow away from the gastric remnant.

Aberrant activation of histone lysine-specific demethylase (LSD1) increases tumorigenicity; hence, LSD1 is considered a therapeutic target for various human cancers. Although melatonin, an endogenously produced molecule, may defend against various cancers, the precise mechanism involved in its anti-oral cancer effect remains unclear. Patient-derived tumor xenograft (PDTX) models are preclinical models that can more accurately reflect human tumor biology compared with cell line xenograft models. Here, we evaluated the anticancer activity of melatonin by using LSD1-overexpressing oral cancer PDTX models. By assessing oral squamous cell carcinoma (OSCC) tissue arrays through immunohistochemistry, we examined whether aberrant LSD1 overexpression in OSCC is associated with poor prognosis. We also evaluated the action mechanism of melatonin against OSCC with lymphatic metastases by using the PDTX models. Our results indicated that melatonin, at pharmacological concentrations, significantly suppresses cell proliferation in a dose- and time-dependent manner. The observed suppression of proliferation was accompanied by the melatonin-mediated inhibition of LSD1 in oral cancer PDTXs and oral cancer cell lines. In conclusion, we determined that the beneficial effects of melatonin in reducing oral cancer cell proliferation are associated with reduced LSD1 expression in vivo and in vitro.

Background and Aim The aim of this study is to evaluate the association of the regulatory T cells (Treg)/T‐helper (Th) 17 cells and transforming growth factor‐β1 (TGF‐β1)/interleukin‐17 (IL‐17) ratios with the survival and disease progression in patients with hepatitis B virus (HBV)‐associated liver cirrhosis (LC). Methods The frequencies of Treg and Th17 cells were analyzed in 28 patients with HBV‐LC, 70 patients with chronic hepatitis B (CHB) and 20 normal controls (NC) by flow cytometry. The levels of cytokines related to Treg/Th17 differentiation, including IL‐10, TGF‐β1, IL‐17, and IL‐23, were measured by ELISA. Results Compared with NC, Treg cells were significantly increased in CHB patients and slightly increased in HBV‐LC patients, whereas Th17 cells were markedly increased both in patients with CHB and HBV‐LC. HBV‐LC patients, especially the nonsurvival ones, manifested a profound decrease in the Treg/Th17 ratio, which was negatively correlated with Child‐Pugh and model of end‐stage liver disease scores. Serum IL‐10, TGF‐β1, IL‐17, and IL‐23 levels were all significantly higher in HBV‐LC patients than in NC. In addition, the TGF‐β1/IL‐17 ratio was also markedly increased in patients with HBV‐LC, especially in nonsurvival and decompensated liver cirrhosis patients, and positively correlated with total bilirubin, Child‐Pugh, and model of end‐stage liver disease scores. Conclusions The decreased Treg/Th17 ratio and increased TGF‐β1/IL‐17 ratio may be associated with the survival and disease progression in HBV‐LC patients, and both of the two ratios can be used independently to predict the prognosis and disease progression of HBV‐LC patients.

Diagnosis and management of rudimentary horn pregnancy remain a challenge. We should be alert to prenatal ultrasound with the intention of making an earlier diagnosis, thereby resulting in decreased maternal morbidity and mortality.

Triptolide, a diterpenoid triepoxide derived from the Chinese herb Tripterygium wilfordii, exerts an antitumor effect in KB cancer cells through the induction of apoptosis. In this study, we show that triptolide possesses an anticancer effect on drug-sensitive parental KB cells and multidrug-resistant KB-7D and KB-tax cells that overexpress multidrug resistance protein and MDR, respectively. Our data revealed that triptolide decreases the expression of multidrug resistance protein and MDR in both KB-7D and KB-tax cells. It also induces apoptosis in these multidrug-resistant cancer cells by activating caspase-3, and decreasing Mcl-1 and XIAP. Triptolide not only inhibits tumor growth but also induces apoptosis of these drug-resistant cancer cells in xenograft mouse models. Moreover, we also show that triptolide combined with 5-fluorouracil could be an alternative strategy for chemotherapy enhancement. These results indicate the therapeutic value of triptolide on multidrug-resistant cells, and when combined with 5-fluorouracil for the enhancement of cancer therapy.