The value of MG7-Ag and COX-2 for predicting malignancy in gastric precancerous lesions.

Here we aimed to first investigate the clinical value of combined detection of MG7-Ag and COX-2 (cyclo-oxygenase 2) in prediction of advances in gastric precancerous lesions. Immunohistochemical analysis was used to examine the expression of MG7-Ag and COX-2 in 396 cases of patients with gastric precancerous lesions, including 66 cases of atrophic gastritis, 106 cases of intestinal metaplasia, 174 cases of low-moderate-grade dysplasia and 50 cases of high-grade dysplasia. The relation of MG7-Ag and COX-2 staining with various clinicopathological features was analysed by follow-up study.

Monoclonal antibodies MC3 and MC5 can be used as a tool for screening colorectal cancer.

MC3 and MC5 are both colorectal cancer-specific MAbs previously prepared in our laboratory that can detect colorectal cancer with high sensitivity and specificity. Thus far the distribution of MC3-Ag and MC5-Ag in colorectal cancer remains largely unknown. In the present study, we have firstly found that the expression of MC3-Ag and MC5-Ag was higher in moderate-differentiated and poor-differentiated colorectal cancer tissue than that in well-differentiated colorectal cancer tissue by immunohistochemistry.

Depression of MAD2 inhibits apoptosis and increases proliferation and multidrug resistance in gastric cancer cells by regulating the activation of phosphorylated survivin.

Mitotic arrest-deficient 2 (MAD2) is one of the essential mitotic spindle checkpoint regulators, and it can protect cells from aberrant chromosome segregation. The Mad2 gene is very rarely mutated in many kinds of human cancer, but aberrantly reduced expression of MAD2 has been correlated with defective mitotic checkpoints in several human cancers. We have previously found that the MAD2 expression level is also shown to be associated with the multidrug resistance of tumour cells.

Decreased expression of CIAPIN1 is correlated with poor prognosis in patients with esophageal squamous cell carcinoma.

Background: CIAPIN1, a newly identified antiapoptotic molecule, is a downstream effector of the receptor tyrosine kinase-Ras signaling pathway in the mouse Ba/F3 pro-B cell line. Neither CIAPIN1 expression nor its clinical significance has been previously examined in esophageal squamous cell carcinoma (ESCC), and the present immunohistochemical analysis is the first study on CIAPIN1 distribution in ESCC.

Aims: To investigate the relationships between the expression of CIAPIN1 and clinicopathological characteristics of ESCC, and evaluate the relationship between the expression of this gene and prognosis in ESCC patients.

New insights into the mechanisms of gastric cancer multidrug resistance and future perspectives.

Gastric cancer is still the second leading cause of cancer death worldwide. Chemotherapy is one of the major treatment options for advanced gastric cancer. The efficacy of chemotherapy for gastric cancer is poor due to insensitivity and the development of multidrug resistance (MDR).

CIAPIN1 as a therapeutic target in cancer.

Importance Of The Field: Cytokine-induced apoptosis inhibitor 1 (CIAPIN1) is a newly identified cytokine-induced apoptosis inhibitor, which has roles in cell division and angiogenesis. Owing to its prognostic value for human tumors and involvement in cancer progression and tumor cell resistance to anticancer agents, CIAPIN1 has been proposed as an attractive target for new anticancer interventions.

Areas Covered In This Review: We define CIAPIN1's potential function as a new therapeutic target for anticancer interventions and this review covers all related literature on CIAPIN1 in cancer from the past 5 years

What The Reader Will Gain: Several preclinical studies have demonstrated that CIAPIN1 is associated with chemotherapy resistance, increased tumor recurrence and shorter patient survival in different human tumor models, making anti-CIAPIN1 therapy an attractive cancer treatment strategy.

MiR-218 inhibits invasion and metastasis of gastric cancer by targeting the Robo1 receptor.

MicroRNAs play key roles in tumor metastasis. Here, we describe the regulation and function of miR-218 in gastric cancer (GC) metastasis. miR-218 expression is decreased along with the expression of one of its host genes, Slit3 in metastatic GC.

Monoclonal antibody MG7 as a screening tool for gastric cancer.

MG7 is a gastric cancer-specific MAb with high specificity and sensitivity. By using MG7 MAb, we found that MG7Ag was increasingly detected in superficial gastritis, atrophic gastritis, intestinal metaplasia, atypical hyperplasia, and gastric cancer, indicating that MG7Ag could be considered an important early warning molecule of gastric cancer and MG7 MAb could be used as a tool for screening gastric cancer. We have developed a new and sensitive system, immuno-realtime PCR, for detection of MG7Ag in the serum.

Ribosomal protein L6 promotes growth and cell cycle progression through upregulating cyclin E in gastric cancer cells.

Our previous study revealed that human ribosomal protein L6 (RPL6) was upregulated in multidrug-resistant gastric cancer cells and over-expression of RPL6 could protect gastric cancer cells from drug-induced apoptosis. The present study was designed to explore the role of RPL6 in tumorigenesis and development of gastric cancer. The expression of RPL6 in gastric cancer tissues and normal gastric mucosa was evaluated by immunohistochemical staining.

Screening and identification of recombinant anti-idiotype antibodies against gastric cancer and colon cancer monoclonal antibodies by a phage-displayed single-chain variable fragment library.

Several monoclonal antibodies (McAbs) have been developed that show high sensitivity and specificity to gastric cancer and colorectal cancer. However, few of the antigens recognized by these antibodies have been identified. The authors now report the selection of anti-idiotype (anti-id) antibodies of MGb1 McAb against gastric cancer and MC5 McAb against colorectal cancer using phage-displayed single-chain variable fragment (ScFv) libraries.

Proteasome inhibition: a new therapeutic strategy to cancer treatment.

The ubiquitin-proteasome system is a major pathway for protein degradation. Targeting this pathway using proteasome inhibitors represents a novel approach for the treatment of cancer. Proteasome inhibitors lower cell proliferation and induce apoptosis in solid and hematologic malignancies through multiple mechanisms, including stabilization of cell cycle regulators and pro-apoptotic factors, stimulation of bone morphogenetic protein signaling, inhibition of protein translation, and sensitization to ligand-induced apoptosis.

IkappaBalpha polymorphism at promoter region (rs2233408) influences the susceptibility of gastric cancer in Chinese.

Background: Nuclear factor of kappa B inhibitor alpha (I kappaB alpha) protein is implicated in regulating a variety of cellular process from inflammation to tumorigenesis. The objective of this study was to investigate the susceptibility of rs2233408 T/C genotype in the promoter region of I kappaB alpha to gastric cancer and the association of this polymorphism with clinicopathologic variables in gastric cancer patients.

Methods: A population-based case-control study was conducted between 1999 and 2006 in Guangdong Province, China.

Macroautophagy and ERK phosphorylation counteract the antiproliferative effect of proteasome inhibitor in gastric cancer cells.

The ubiquitin-proteasome system and macroautophagy are two complementary pathways for protein degradation. Emerging evidence suggests that proteasome inhibition might be a promising approach for the treatment of cancer. In this study, we show that proteasome inhibitor MG-132 suppressed gastric cancer cell proliferation and induced macroautophagy.

MiR-150 promotes gastric cancer proliferation by negatively regulating the pro-apoptotic gene EGR2.

Accumulating evidence suggests small non-coding RNAs (microRNAs) play important roles in human cancer progression. In the present study, we found miR-150 was overexpressed in gastric cancer cell lines and tissues. Ectopic expression of miR-150 promoted tumorigenesis and proliferation of gastric cancer cells.

Inhibition of the p53-MDM2 interaction by adenovirus delivery of ribosomal protein L23 stabilizes p53 and induces cell cycle arrest and apoptosis in gastric cancer.

Background: Inhibiting MDM2 activity in tumors that express wild-type (wt) p53 but have high levels of MDM2 protein has been considered an attractive anticancer strategy for many years. Previous studies revealed that human ribosomal protein L23 (RPL23) inhibited MDM2-mediated p53 degradation and thus induced p53 levels as well as its activity, suggesting that it might be a candidate for use as a gene therapy for cancer. In the present study, we evaluated whether targeting this pathway could be of therapeutic value against human gastric carcinoma.

ERK/MAPK activation involves hypoxia-induced MGr1-Ag/37LRP expression and contributes to apoptosis resistance in gastric cancer.

We previously demonstrated that hypoxia increased the hypoxia-inducible factor (HIF-1)-dependent MGr1-Ag/37LRP expression, which enhanced adhesion of gastric cancer cells to laminin, inhibited drug-induced apoptosis and caused cell adhesion-mediated drug resistance (CAM-DR). Here, we investigated the role of extracellular-regulated kinase (ERK) 1/2 in the signaling mechanisms underlying these events. We found that hypoxia activated ERK activity in vitro and in vivo.

[Transjugular intrahepatic portosystemic shunt and combination with percutaneous transhepatic or transsplenic approach for the treatment of portal vein thrombosis with or without cavernomatous transformation].

Objective: To evaluate retrospectively the feasibility, efficacy and safety of transjugular intrahepatic portosystemic shunt (TIPS) or percutaneous transhepatic or transsplenic approach to the portal vein with the combination of TIPS for the treatment of patients with portal vein thrombosis with or without cavernous transformation.

Methods: Sixty-five patients with portal vein thrombosis from July 2002 to August 2007 at our hospital were analyzed retrospectively. Indirect portography through superior mesenteric artery was performed to determine the approaches for TIPS procedure.

Potent inhibition of human gastric cancer by HER2-directed induction of apoptosis with anti-HER2 antibody and caspase-3 fusion protein.

Background And Aims: HER2, an oncogene, has been found to be over-expressed in 10-40% of human gastric carcinomas. The aims of this study were to investigate if a fusion protein consisting of anti-HER2 sFv and constitutively active caspase-3 was capable of inducing apoptosis in HER2-expressing human gastric cancer cells and blocking the growth of human gastric cancer xenografts in nude mice.

Methods: NIH3T3 cells stably transduced with the pcDNA3.

Survival prediction of gastric cancer by a seven-microRNA signature.

Aims: Several microarray studies have reported microRNA (miRNA) expression signatures that classify cancer patients into different prognostic groups. No study has evaluated the association between miRNA expression patterns and gastric cancer prognosis. In this study, we developed a seven-miRNA signature that is closely associated with survival of patients with gastric cancer.