Biomedical subjects

Y M Jeon

Publications and source records attributed to Y M Jeon.

5 recordsLinked to original sources

PubMed2000

Genetic alterations of gastric cancer: comparative genomic hybridization and fluorescence In situ hybridization studies.

Genetic changes leading to the development of gastric cancers are still in dispute. In the following study, we used comparative genomic hybridization (CGH) to screen for DNA copy number changes along all chromosomes in 37 gastric carcinomas, and fluorescence in situ hybridization (FISH) with the C-MYC and TP53 probes in 14 cases for comparison. The aim of this study was to identify those chromosome regions that contain genes important for the development of gastric carcinomas and to identify genetic markers associated with tumor progression. The most often involved gains were 2q, 7pq, 8pq, 13q, 17q, 18q, and 20pq. The most commonly deleted regions were 17p. The pattern of genetic changes was different depending on the existence of nodal metastasis and histologic types. Gains in 8q and losses in 17p were the most common features of the CGH changes. However, only 3 among the available 10 cases (30%) showed an amplification of the C-MYC gene by FISH. Allelic loss of TP53 was found in 2 of 4 cases (50%). This difference might be due to another rearrangement of these 2 genes which cannot be detected by FISH, or other possible genes in that area may be involved in the tumorigenesis and nodal metastasis of gastric carcinomas.

Adenocarcinoma↗

PubMed1999

Detection of genetic alterations in bladder tumors by comparative genomic hybridization and cytogenetic analysis.

Comparative genomic hybridization (CGH) and conventional cytogenetic karyotyping were used to screen for losses and gains of DNA sequences along all chromosome arms in 16 bladder tumors. Cytogenetic results were highly complex. The most frequently affected chromosomes were 5, 8, 9, 21, and Y as determined by karyotyping. There was close correlation between the CGH data and cytogenetic results in near-diploid tumors with simple karyotypes. However, some unexpected results were observed by CGH in tumors with several composite clones. Common amplification of copy numbers of DNA sequences by CGH were seen at 1q, 3q, 4q, 5p, 6p/q, 7p, 8q, 11q, 12q, 13q, 17q, 18q, and 20p/q (more than 20% of cases). High level amplification was noted at 1p32, 3p21, 3q24, 4q26, 8q21-qter, 11q14-22, 12q15-21, 12q21-24, 13q21-31, 17q22, and 18q22. Deletions were noted at 2q21-qter. 4q13-23, 5q, 8p12-22, 9p/q, and 11p13-15 (more than 20% of cases). Although most amplifications and deletions have been previously described in the literature, our study showed some intriguing and uncommon regions, different from those found in past studies. These were the amplification of 7p, 8q, 11q14-qter 12q24-24, 13q21-31, and 18q22, and deletion on 4q13-23, even though loss of heterozygosity was not detected at this locus. In spite of the very complex pattern of genetic changes in bladder tumors, most of these uncommon aberrations have to be implicated in bladder tumors, and further molecular genetic methods are necessary to establish whether the chromosomal regions contain candidate genes which contributed to the initiation and progression of bladder tumors.

Aged↗

PubMed1999

Receptor activator of NF-kappaB recruits multiple TRAF family adaptors and activates c-Jun N-terminal kinase.

Receptor activator of NF-kappaB (RANK) is a recently cloned member of the tumor necrosis factor receptor (TNFR) superfamily, and its function has been implicated in osteoclast differentiation and dendritic cell survival. Many of the TNFR family receptors recruit various members of the TNF receptor-associated factor (TRAF) family for transduction of their signals to NF-kappaB and c-Jun N-terminal kinase. In this study, the involvement of TRAF family members and the activation of the JNK pathway in signal transduction by RANK were investigated. TRAF1, 2, 3, 5, and 6 were found to bind RANK in vitro. Association of RANK with each of these TRAF proteins was also detected in vivo. Expression of RANK in cultured cells also induced the activation of JNK, which was blocked by a dominant-negative form of JNK. Furthermore, by employing various C-terminal deletion mutants of RANK, the regions responsible for TRAF interaction and JNK activation were identified. TRAF5 was determined to bind to the C-terminal 11 amino acids and the other TRAF members to a region N-terminal to the TRAF5 binding site. The domain responsible for JNK activation was localized to the same region where TRAF1, 2, 3, and 6 bound, which suggests that these TRAF molecules might mediate the RANK-induced JNK activation.

Amino Acid Sequence↗

PubMed1999

Facial warming increases the threshold for shivering.

A decrease of 1-2 degrees C core temperature provides protection against cerebral ischemia. However, shivering usually prevents reduction in core temperature in unanesthetized patients. Therefore, it was tested whether facial and airway heating increases the shivering threshold and enables core cooling in unanesthetized patients. Nine trials were performed on seven healthy male volunteers. Each subject was positioned supine on a circulating-water mattress (8-15 degrees C) with a convective-air coverlet (15-18 degrees C) extending from the neck to the feet. A dynamic study protocol governed by individualized physiological responses was used. Focal facial (and airway) warming was employed to suppress involuntary motor activity (muscle tensing, shivering) and, thereby, enabling noninvasive cooling to lower the core temperature. The following parameters were monitored: 1) heart rate, 2) blood pressure, 3) core temperature (tympanic, axilla, and rectal), 4) cutaneous temperatures, and 5) a subjective shiver index (scale 1-10). In three, electromyograms and infrared thermographs were also obtained. Upon cooling without facial and airway warming, involuntary motor activity increased until it was widespread. This vigorous motor activity prevented any significant lowering of core temperature or caused it to slightly increase. Subsequently, in all subjects, within seconds after the application of facial focal warming, motor activity was suppressed almost completely, and within minutes core temperatures significantly decreased. Preliminary studies described here indicate that focal facial warming applied during active whole body cooling to initiate mild hypothermia might minimize the need to pharmacologically suppress involuntary motor activity. Such a procedure might be useful for initiating as soon as possible (such as during emergency transport), cerebral mild hypothermia in order to maximize protection and thus improve outcome in neurologically injured patients (head trauma, stroke).

Adult↗

PubMed1995

Characterization of cell lines established from human hepatocellular carcinoma.

We characterized 8 human hepatocellular-carcinoma cell lines established from the primary tumors of Korean patients. All lines showed substrate adherence and one line from anaplastic tumor also grew as floating aggregates. Most cultured cells maintained many morphological characteristics of the original tumors from which they were derived. Doubling times varied from 34 to 72 hr. All lines showed relatively high viability and were not contaminated with Mycoplasma or bacteria. All lines showed aneuploidy and were proven to be unique by DNA fingerprinting analysis. Hepatitis-B-virus (HBV) DNA was integrated in the genomes of all lines. Two of the cell lines (SNU-354, SNU-368) showed expression of HBV and HBVx (HBx) transcripts. SNU-354 strongly expressed albumin, and SNU-368 expressed transferrin and insulin-like growth factor II. No lines produced alpha-fetoprotein at the RNA and protein level. These cell lines represent useful tools for in vitro studies related to hepatocellular carcinoma.

Adult↗