Publications by authors named "Chang-qing Su"

Aim:   There is no clear consensus on the optimal timing of surgical resection for synchronous colorectal liver metastases (SCLM). This study is a meta-analysis of the available evidence.

Methods:   Systematic review and meta-analysis of trials comparing outcomes following simultaneous resection with staged resection for SCLM published from 1990 to 2010 in PubMed, Embase, Ovid and Medline.

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Objective: To investigate the relationship between p16 expression and cell proliferation and prognosis in gastric cancer patients.

Methods: Gastric cancer cell lines SGC-7901, MKN45, MKN28, human embryonic kidney cell line HEK293, human fibroblast cell line MRC-5, and surgical specimens of gastric carcinoma and adjacent normal gastric mucosa from 65 patients were included in this study. RT-PCR, MTT and FCM assays were used to detect p16 expression in gastric cancer cell lines and surgical specimens of gastric cancer.

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Objective: To establish a human gallbladder carcinoma cell line derived from a metastatic gallbladder carcinoma and identify its biological characteristics.

Methods: Tissue samples were separated from the surgical specimen obtained from a patient with metastatic carcinoma and single-cell suspension was prepared. Then the cells were cultured in DMEM medium supplemented with 15% fetal bovine serum.

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Article Synopsis
  • - The study aims to create an advanced microarray for high-speed detection of key gene mutations (p53, p16, Rb, and EGFR) linked to non-small-cell lung cancer (NSCLC) for better molecular diagnosis.
  • - Researchers developed specific probes for these mutations, analyzing genomic DNA from cancer and normal lung tissue samples, finding significant mutation rates in NSCLC specimens compared to normal tissues.
  • - The new microarray showed high sensitivity (81.5%) and specificity (90%) in detecting mutations, indicating its potential to enhance NSCLC diagnosis and inform targeted therapies.
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The authors present the case of a 48-year-old man with hepatitis B cirrhosis, who developed two primary malignant liver tumors that were morphologically distinct from each other. The first tumor was a hepatocellular carcinoma and the second tumor, detected 17 months later was a hepatic carcinosarcoma with cholangiocarcinomatous and sarcomatous components, without any hepatocellular carcinoma component. Clonality studies using microsatellite-based loss of heterozygosity (LOH) demonstrated different LOH patterns existed between the hepatocellular carcinoma and the hepatic carcinosarcoma, indicative of different clonal origins.

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Aim: Gene therapy represents a promising therapeutic strategy for hepatocellular carcinoma (HCC). To improve the ratio of killing efficacy on tumor cells to side-effect on normal cells, we constructed an oncolytic adenovirus vector, AdSu-hE, expressing the human endostatin (hE) gene, in which the chimeric promoter of human epidermal growth factor receptor 2 enhancer and human telomerase reverse transcriptase promoter was used to control the adenoviral E1a gene.

Methods: Tumor-selective replication of adenovirus AdSu-hE and its concomitant expression of endostatin were measured by 50% tissue culture infective dose method, fluorescent protein expression, Western blot and enzyme linked immunosorbent assay in cancer and normal cell lines.

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Objective: To construct a RU486 inducible recombinant adenovirus of murine IL-12 protein and study its effect and safety on colonic cancer.

Methods: The replication-defective recombinant adenovirus were produced after cotransfection of shutter vector pDC-RUmIL-12 and adenovirus DNA helper plasmid pBHGloxDeltaE1, 3Cre into HEK293 cells. The recombined adenovirus was purified by CsCl density gradient centrifugation and its titer was determined by end point dilution assay.

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Conditionally-replicating adenovirus (CRAd) therapy is currently being tested against pancreatic cancer and has shown some promise. To improve the efficacy, a novel virus CRAd-Cans was designed by deletion of E1B-55kDa gene for selective replication in tumor cells, as well as carrying a new angiogenesis inhibitor gene, canstatin. CRAd-Cans mediated higher expression of canstatin in BxPC-3 pancreatic cancer cell line compared to the replication-deficient adenovirus Ad5-Cans.

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Objective: To construct an inducible eukaryotic vector carrying red fluorescent protein (DsRed) and evaluate the regulation of DsRed gene expression in vitro.

Methods: The vector pRS17-RUDsRed containing DsRed gene, promoter and RU486-inducible system was constructed using molecular biological methods. To minimize potential interference, the two transcriptional elements were spaced with a 1.

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Aim: To evaluate the therapeutic efficiency of replicative adenovirus CNHK300 targeted in telomerase-positive hepatocellular carcinoma.

Methods: CNHK300, ONYX-015 (55 kDa protein deleted adenovirus) and wtAd5 (wild type adenovirus 5) were compared, and virus proliferation assay, cell viability assay, Western blot and fluorescence microscopy were used to evaluate the proliferation and cytolysis selectivity of CNHK300.

Results: The replicative multiples in Hep3B and HepG II after 48 h of CNHK300 proliferation were 40625 and 65326 fold, respectively, similar to that of wtAd5.

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Objective: To investigate the anti-tumor effect of a novel gene-viral therapeutic system CNHK300-murine endostatin (CNHK300-mE) on gastric cancer.

Methods: SGC-7901 gastric cancer cells (5 x 10(7) cells/mouse) were injected s.c.

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Aim: To construct a tumor-selective replication-competent adenovirus (RCAd), SG300, using a modified promoter of human telomerase reverse transcriptase (hTERT).

Methods: The antitumor efficacy of SG300 in hepatocellular carcinoma was assessed in vitro and in vivo. In vitro cell viability by MTT assay was used to assess the tumor-selective oncolysis and safety features of SG300, and in vivo antitumor activity of SG300 was assessed in established hepatocellular carcinoma models in nude mice.

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Objective: To develop a novel vector system, which combines the advantages of the gene therapy, antiangiogenic therapy and virus therapy, and to observe its effect on lung cancer.

Methods: Human angiostatin gene hA(k1-5) was inserted into the genome of the replicative virus specific for the tumor cells by virus recombination technology. The expression of hA(k1-5), its effect on tumor growth in vitro and in vivo were studied.

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Objective: To evaluate the therapeutic efficiency of replicative adenovirus CNHK300 targeted at telomerase-positive hepatocellular carcinoma.

Methods: Human liver cancer cell line HepGII and Hep3B, human embryonic kidney cell line 293, and normal human fibroblasts of the line BJ were cultured and added with adenoviruses CNHK300, ONYX-015 (55 000 protein deleted adenovirus), or wtAd5 (wild type 5) with different multiplicity of infection (MOI) for 7 days. 293 cells were used to measure the titer of the filial generation virus from different cells.

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Objective: To investigate the anti-tumor effects of a novel gene-viral therapeutic system CNHK300-murine endostatin (CNHK300-mE) in hepatocellular carcinoma (HCC).

Methods: A novel gene-viral therapeutic system named CNHK300-mE was constructed by employing the human telomerase reverse transcriptase (hTERT) promoter to drive the expression of adenovirus E1A gene and cloning the therapeutic gene murine endostatin (mE) into the adenovirus genome. Hepatocellular cells of the HepGII and Hep3B lines and normal fibroblasts of the MRC-5 line were cultured and infected with the viruses CNHK300-mE, ONYX-015, replicative adenovirus without therapeutic gene, and Ad-mE, non-replicative adenovirus with the same therapeutic gene.

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Objective: To study the inhibitory effect of retroviral packaging cells injected intrasplenically encoding mouse interleukin-12 (mIL-12) and human interleukin-2 (hIL-2) fusion gene on the growth of hepatocellular carcinoma.

Methods: The retroviral vectors encoding mIL-12 gene, hIL-2 gene, and mIL-12 and hIL-2 genes, GCIL12EXPN, GCXEIL2PN, and GCIL12EIL2PN were constructed and then transfected into the retroviral packaging cells PA317 to construct cells PA317-GCIL12EXPN, PA317-GCXEIL2PN, and PA317-GCIL12EIL2PN. Rat hepatocellular carcinoma cells CBRH3 were implanted into the livers of Wistar rats to establish hepatoma animal model.

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