科创中国

Li Xiaohua;Wu Kaichun;Fan Daiming

Hepatology Baltimore Md

2009

Li Xiaohua;Wu Kaichun;Fan Daiming

Hepatology

2009

To evaluate gastric carcinoma-associated antigen, MG7-Ag, for detection of gastric cancer in a high-risk population, a population-based screening of gastric cancer was conducted in Linqu County, Shandong Province, China. In 2002 and 2003, a total of 2,710 participants aged 35-65 years received an endoscopic examination with 5 biopsies taken from standard sites with pathological diagnosis, and serum samples were collected to detect MG7-Ag by serum-based Immunopolymerase chain reaction (PCR) assay. The sensitivity and specificity of MG7-Ag Immuno-PCR assay in detecting of gastric cancer were assessed. Of 2,710 participants, 148 (5.46%) were determined to be MG7-Ag positive. The sensitivity of MG7-Ag Immuno-PCR assay for the detection of gastric cancer was 77.5% (31 of 40 gastric cancer cases), the specificity was 95.62% (2,553 of 2,670 nongastric cancer subjects) and the accuracy was 73.12%. A total of 24 gastric cancer cases were in Stage I or II, of which 17 (70.8%) were MG7-Ag positive. However, the proportion of MG7-Ag positivity in subjects with superficial gastritis, chronic atrophic gastritis, intestinal metaplasia, indefinite dysplasia or dysplasia was ranged from 3.00% to 5.61% in comparison with 77.5% in those with gastric cancer. Our findings suggest that MG7-Ag was a sensitive and specific serum biomarker and may have a potential for gastric cancer screening in the high-risk population. © 2009 UICC.

Zhang Lian;Ren Jun;Pan Kaifeng;Ma Junling;Li Jiyou;Shen Lin;Zhang Xiaodong;Li Jie;You Weicheng;Fan Daiming;Gail Mitchell

International Journal of Cancer

2010

Background Infliximab was approved for use in ulcerative colitis in recent years. It has been debated if infliximab increases the risk of post-operative complications in patients with ulcerative colitis. Aim To perform a meta-analysis that examines the relationship between preoperative infliximab treatment and short-term post-operative complications in patients with ulcerative colitis. Methods We searched the PubMed and MEDLINE databases to identify observational studies on the impact of pre-operative infliximab use on short-term post-operative complications in ulcerative colitis. Infectious complications mainly included wound infection, sepsis and abscess, whereas non-infectious complications included intestinal obstruction, thromboembolism and gastrointestinal haemorrhage. Pooled odds ratios (ORs) were calculated for each relationship. Results A total of 5 studies and 706 patients were included in our meta-analysis. Overall, we did not find a strong association between pre-operative treatment of infliximab and short-term infectious [OR 2.24, 95% confidence interval (CI) 0.63-7.95] or non-infectious (OR 0.85, 95% CI 0.50-1.45) post-operative complications in ulcerative colitis patients. On the contrary, we discovered that pre-operative infliximab use increased short-term total post-operative complications (OR 1.80, 95% CI 1.12-2.87). Conclusions Pre-operative infliximab use increased the risk of short-term post-operative complications. Subgroup analysis is underpowered to assess the nature of these complications but shows a trend towards increased post-operative infection. © 2010 Blackwell Publishing Ltd.

Yang Z.;Wu Q.;Wu K.;Fan D.

Alimentary Pharmacology and Therapeutics

2010

Qi Xingshun;Han Guohong;Fan Daiming

Hepatology

2010

Nonsteroidal anti-inflammatory drugs (NSAIDs) can inhibit cell growth and metastasis, and induce cell apoptosis in cancerous cells. They have been shown to reduce incidence and mortality of gastric cancer by an unknown mechanism. NSAIDs often exert their effects by Cox-2 inhibition, and Cox-2 is overexpressed in gastric cancer cells. Nevertheless, when gastric cancer cells were treated with different NSAIDs, the non-Cox-2-inhibiting R-flurbiprofen was most effective at reducing proliferation of gastric cancer cells in vitro. R-Flurbiprofen prevented the metastatic characteristics of gastric cancer cells in vitro, and reduced tumor size and metastasis in vitro, when gastric cancer cells were injected into nude mice. R-Flurbiprofen also affected multidrug resistance, increasing the sensitivity of resistant gastric cancer cells to chemotherapeutic agents. Mechanistically, R-flurbiprofen was found to have pleiotropic effects, changing levels of cell cycle factors like Cyclin D1 and CKD4, apoptotic protwins like caspase3 and Bcl-2, and protwins that affect metastasis, like metalloproteases. Consistent with reports on other cancer cell types, NSAID treatment with R-flurbiprofen increased levels of the tumor suppressor neurotrophin receptor (p75 ^NTR ) in gastric cancer cells. The anticancer effects of R-flurbiprofen were found to require induction of p75 ^NTR via the p38 signaling pathway, suggesting a possible mechanism of action. © 2010 American Chemical Society.

Jin Haifeng;Liu Lili;Gao Liucun;Sun Li;Li Xiaohua;Pan Yanglin;Shi Hai;Wu Kaichun;Fan Daiming;Wang Zhipeng;Liu Na;Hong Liu;Liang Jie;Wu Qiong;Yang Zhiping;Zhao Hongxi

Molecular Pharmaceutics

2010

Li Xiaohua;Wu Kaichun;Fan Daiming;Zhang Ying

Hepatology

2010

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. In this connection, proteasome inhibition activates macroautophagy, a compensatory protein degradation system, as well as other pro-survival signaling pathways. Inhibition of these auto-protective responses sensitizes cancer cells to the anti-proliferative effects of proteasome inhibitors. © 2009 Elsevier Ireland Ltd.

Wu William Ka Kei;Cho Chi Hin;Lee Chung Wa;Yu Jun;Yiu Sung Joseph Jao;Wu Kaichun;Fan Daiming

Cancer Letters

2010

Background Tumour necrosis factor alpha (TNF-α) is involved in the pathogenesis of Crohn's disease (CD). However, results on the association between the polymorphisms in TNF-α promoter and the risk of CD are inconsistent. Aim To perform a quantitative synthesis for the genetic polymorphisms in TNF-α promoter and CD risk. Methods Databases were searched (up to 2009) and 31 studies were included. Risks of CD associated with the polymorphisms in TNF-α promoter were assessed. Results Overall, individuals with -1031 TC+CC genotype had a slightly increased risk to develop CD compared with individuals with -1031 TT genotype (OR, 1.32; 95% CI, 1.03-1.70). In the further stratified analysis, we found Asians with the -1031T>C, -863 C>A and -857 C>T variant polymorphisms have almost one and a half CD risk compared with other genotypes (OR, 1.58; 95% CI, 1.16-2.15; OR, 1.55; 95% CI, 1.18-2.02; OR, 1.54; 95% CI, 1.19-1.99 respectively). We did not find -308 G>A variant associated with CD location and disease behaviours in stratified analysis. Conclusions TNF-α polymorphisms in the promoter region might be used as a biomarker for CD risk prediction. Larger studies with mixed ethnicity subjects and stratified by clinical and sub clinical characteristics are needed to validate our findings. © 2010 Blackwell Publishing Ltd.

Han Z.;Li C.;Han S.;Han Y.;Qiu J.;Shi Y.;Wang J.;Sun A.;Ding J.;Wu K.;Fan D.

Alimentary Pharmacology and Therapeutics

2010

Purpose: Epithelial cellular adhesion molecule (EpCAM) is an attractive immunotherapeutic target to overcome metastasis of a variety of epithelium-oriented cancers. Edrecolomab, one kind of EpCAM monoclonal antibody (Panorex^®), has been approved for clinical application as postoperative adjuvant therapy in breast and colorectal cancer. However, the role of EpCAM in gastric cancer metastasis remains unclear. Results: EpCAM was found to be more highly overexpressed in metastatic gastric cancer than in nonmetastatic samples by immunohistochemistry staining. The expression level of EpCAM in gastric cancer cell lines was determined by reverse-transcription polymerase chain reaction (RT-PCR) and Western blotting, respectively. Downregulation of EpCAM by small interfering RNA (siRNA) significantly suppressed in vitro adhesive, invasive, and migratory and in vivo metastatic abilities of gastric cancer cells. Conclusion: We provide first evidence that EpCAM contributes to the migration of gastric cancer, suggesting that EpCAM-targeted therapy might be a promising strategy in metastatic gastric cancer. © 2009 Springer Science+Business Media, LLC.

Du Wenqi;Cao Shanshan;Wang Li;Bai Feihu;Liu Jie;Fan Daiming;Ji Hongzan

Digestive Diseases and Sciences

2010