• Proceedings of the Korean Society of Toxicology Conference
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• 2002.11b
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• pp.196-196
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• 2002

p16INK4a tumor suppressor gene transfer in the non-small cell lung cancer cells by transduction of recombinant adenovirus (Ad5CMV-p16) resulted in significant inhibition of cancer cell growth (Anticancer Res., 1998, 18:3257-3261). As a safety concern, we have investigated gene and protein expression after transduction of adenoviral vector (Ad5CMV-p16) in human non-small cell lung cancer (A549) cells by using microarray and 2D gel electrophoresis/ MALDI-TOF.(omitted)

• Proceedings of the PSK Conference
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• 2000.10a
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• pp.165.1-165.1
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• 2000

• Proceedings of the Korea Environmental Mutagen Society Conference
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• 2001.10b
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• pp.191-192
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• 2001

• Proceedings of the Korean Society of Toxicology Conference
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• 2005.05a
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• pp.121-121
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• 2005

• Proceedings of the Korean Society of Toxicology Conference
• /
• 2001.10a
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• pp.191-192
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• 2001

Although the incidence rates of gastric cancer and liver cancer, the most common cancers in Korea, are tending decrease, lung cancer is on the increase every year as cause of cancer death as well as incidence rate in Korea. And cigarette smoke is believed to be responsible for 90% of lung cancer. Many investigators have reported an association between genetic polymorphism of cytochromes P-450 (CYPs) or glutathoine S-transferase (GSTs) and susceptibility to lung cancer.(omitted)

• Proceedings of the Korea Environmental Mutagen Society Conference
• /
• 2002.11a
• /
• pp.196-196
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• 2002

• Proceedings of the Korea Environmental Mutagen Society Conference
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• 2004.11a
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• pp.138-138
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• 2004

• Proceedings of the PSK Conference
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• 2002.10a
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• pp.291.2-291.2
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• 2002

For the safety evaluation of adenovirus-mediated gene therapy. we have investigated gene and protein expression after transduction of adenoviral vector (Ad5CMV-p16) which contains tumor suppressor gene. p161NK4$\alpha$ in human non-small cell lung cancer (A549) cells. We compared the differential gene expression level in the A549 cells treated with Ad5CMV (null type) and Ad5CMV-p16 virus. respectively. by using cDNA membrane chip and oligonucleotide chip. (omitted)

• Proceedings of the Korea Environmental Mutagen Society Conference
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• 2004.11a
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• pp.112-112
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• 2004

• Molecular & Cellular Toxicology
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• v.2 no.4
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• pp.236-243
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• 2006

Microarray analysis of gene expression has become a powerful approach for exploring the biological effects of drugs, particularly at the stage of toxicology and safety assessment. Acetaminophen (APAP) has been known to induce necrosis in liver, but the molecular mechanism involved has not been fully understood. In this study, we investigated gene expression changes of APAP using microarray technology. APAP was orally administered with a single dose of 50 mg/kg or 500 mg/kg into ICR mice and the animals were sacrificed at 6, 24 and 72 h of APAP administration. Serum biochemical markers for liver toxicity were measured to estimate the maximal toxic time and hepatic gene expression was assessed using high-density oligonucleotide microarrays capable of determining the expression profile of >30,000 well-substantiated mouse genes. Significant alterations in gene expression were noted in the liver of APAP-administered mice. The most notable changes in APAP-administered mice were the expression of genes involved in apoptosis, cell cycle, and calcium signaling pathway, cystein metabolism, glutatione metabolism, and MAPK pathway. The majority of the genes upregulated included insulin-like growth factor binding protein 1, heme oxygenase 1, metallothionein 1, S100 calcium binding protein, caspase 4, and P21. The upregulation of apoptosis and cell cycle-related genes were paralleled to response to APAP. Most of the affected gene expressions were returned to control levels after 72 hr. In conclusion, we identified potential hepatotoxicity makers, and these expressions profiling lead to a better understanding of the molecular basis of APAP-induced hapatotoxicity.