Publications by authors named "SungHye Hong"

Thirteen human colorectal cancer (CRC) cell lines were established from 10 primary tumors and 3 metastatic tumors obtained from 13 Korean patients. Characteristics of the cell lines including morphology in vivo and in vitro; mutations of the K-ras, p53, APC and MMR genes and microsatellite instability (MSI) status in vitro were determined. Expression of drug-sensitivity genes including MDR1, MXR, MRP1 and COX2 was also analyzed.

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The telemedicine system aims at monitoring patients remotely without limit in time and space. However the existing telemedicine systems exchange medical information simply in a specified location. Due to increasing speed in processing data and expanding bandwidth of wireless networks, it is possible to perform telemedicine services on personal digital assistants (PDA).

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To evaluate the effect of galectin-3 in cell cycle regulation of colon cancer cells, we looked for binding molecules interacting with galectin-3 and examined the changes in cell cycle by suppressing galectin-3 and the binding molecule. To identify target molecules interacting with galectin-3, we analyzed immunoprecipitate of the anti-galectin-3 antibody obtained from human colon cancer cell line, using matrix-assisted laser desorption ionization-mass spectrometry. We validated subcellular localization of galectin-3 and ATP synthase identified, and ATP synthase activity was determined in the presence of galectin-3.

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Purpose: Calprotectin (heterodimer of calgranulin A and B) has been previously studied as a candidate stool marker for detecting colorectal cancer. We assessed the clinical usefulness of calgranulin B as a stool marker for colorectal cancer in a pilot study of patients with colorectal cancer.

Methods: We performed 2-DE-based proteomics to screen stool markers for colorectal cancer.

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Liver metastasis is a major cause of poor survival of colorectal cancer patients. In order to identify the proteins associated with liver metastasis in colorectal cancer, we carried out two-dimensional gel electrophoresis-based comparative proteomic analysis of normal colon mucosa, primary colon cancer tissue and corresponding metastatic tumor tissue in liver. The proteins identified were further validated by immunohistochemical analysis of 67 quadruplet samples of normal colon primary colorectal cancer and normal liver-synchronous liver metastasis, and 251 colorectal cancers as well as in vitro invasion assay of the human colon cancer cell line, SNU-81.

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Human hepatocellular carcinoma (HepG2) cells take up metallothionein (MT) by endocytosis. MT co-localizes with albumin but not with transferrin, indicating uptake via a non-classical pathway rather than via clathrin-mediated endocytosis. A lipid raft-dependent uptake is indicated by pravastatin inhibition of cholesterol synthesis and methyl-beta-cyclodextrin inhibition of cholesterol translocation to the plasma membrane, reducing MT uptake by 29% and 69%, respectively.

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Purpose: The aim of study was to determine the clinical characteristics and mutational profiles of the mismatch repair genes in hereditary nonpolyposis colorectal cancer (HNPCC) patients with small bowel cancer (SBC).

Experimental Design: A questionnaire was mailed to 55 members of the International Society for Gastrointestinal Hereditary Tumours, requesting information regarding patients with HNPCC-associated SBC and germ line mismatch repair gene mutations.

Results: The study population consisted of 85 HNPCC patients with identified mismatch repair gene mutations and SBCs.

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5-Fluorouracil (5-FU) is widely used for treatment of advanced colorectal cancer. However, it is common for such patients to develop resistance to 5-FU, and this drug resistance becomes a critical problem for chemotherapy. The mechanisms underlying this resistance are largely unknown.

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Hereditary non-polyposis colorectal cancer (HNPCC), the most common hereditary colon cancer syndrome, is a dominant disorder caused by germline defects in mismatch repair (MMR) genes. Identification of MMR gene mutations can have direct clinical implications in counseling and management of HNPCC families. We screened 44 HNPCC and 97 suspected HNPCC Korean families for germline mutations in three MMR genes: MLH1, MSH2 and MSH6.

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It was recently reported that RUNX3 gene expression is significantly downregulated in human gastric cancer cells due to hypermethylation of its promoter region or hemizygous deletion (Cell, 109, 2002). To verify the genetic alterations and methylation status of the RUNX3 gene in colorectal carcinogenesis, we analysed for mutations, loss of heterozygosity (LOH), and RUNX3 gene promoter hypermethylation, in 32 colorectal cancer cell lines. RT-PCR analysis showed undetectable or low RUNX3 expression in 16 cell lines, and no mutations were found in the RUNX3 gene by PCR-SSCP analysis.

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Purpose: 5-Fluorouracil (5-FU) has been the mainstay treatment for colorectal cancer for the past few decades. However, as with other cancers, development of 5-FU resistance has been a major obstacle in colorectal cancer chemotherapy. The purpose of this study was to gain further understanding of the mechanisms underlying 5-FU resistance in colorectal cancer cells.

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Resistance to anticancer drugs is a major obstacle preventing effective treatment of disseminated cancers. Understanding the molecular basis to chemoresistance is likely to provide better treatment. Cell lines resistant to cisplatin or 5-fluorouracil (5-FU) were established from human gastric carcinoma cell lines SNU-638 and SNU-620.

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We have designed a nanosensor to study the potential function of metallothionein (MT) in metal transfer and its interactions with redox partners and ligands by attaching two fluorescent probes to recombinant human MT. The specific labeling takes advantage of two different modification reactions. One is based on the fact that recombinant MT has a free N-terminal amino group when produced by the IMPACT T7 expression and purification system, the other on the observation that one human MT isoform (1b) contains an additional cysteine at position 32.

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