Yong Hyuck Chun

Establishment and characterization of chromosomal aberrations in human cholangiocarcinoma cell lines by cross‐species color banding

Cholangiocarcinoma (CC), a malignant neoplasm of the biliary epithelium, is usually fatal because of difficulty in early diagnosis and lack of availability of effective therapy. Furthermore, little is known about the genetics and biology of CC. Only a few reports concerning cytogenetic studies of CC have been published, and few cell lines have been established. We recently established four CC cell lines, designated as SCK, JCK, Cho‐CK, and Choi‐CK, and report the first application of cross‐species color banding (RxFISH) and multiple chromosome painting for the characterization of the chromosomal rearrangements of these CC cell lines. Each cell line had unique modal karyotypic characteristics and showed a variable number of numerical and structural clonal cytogenetic aberrations. Chromosomes 3, 6, 7, 8, 12, 14, 17, and 18 were commonly involved in structural abnormalities. Homogeneously staining regions were determined in SCK and JCK, and double minute chromosomes were found in Cho‐CK. The chromosomal aberrations of the four CC cell lines were effectively analyzed by RxFISH and FISH with multiple chromosome painting probes. The nonrandom rearrangements suggest candidate regions for isolation of genes related to CC.

Specific plasticity of parallel fiber/Purkinje cell spine synapses by motor skill learning.

New synapse formation may underlie learning and memory. To examine specific synaptic plasticity by motor learning, we conducted quantitative analysis of synapses between parallel fibers and Purkinje cell dendritic spines in cerebella of rats trained to complete various obstacle courses. Synapses between parallel fibers and Purkinje cell spines were classified into single synapse boutons, multiple synapse boutons, and multiple synapse spines by their different contact features. Acrobat-trained animals had more single and multiple synaptic boutons, without change of multiple synapse spines, than motor control animals. These results may suggest that motor learning induces specific synaptogenesis and Purkinje cell spines are primary sites in motor learning-dependent cerebellar synaptic plasticity.

Characterization of chromosomal aberrations in human gastric carcinoma cell lines using chromosome painting

Using chromosome painting, a study of chromosomal abnormalities was performed in six gastric carcinoma cell lines (SNU-484, 601, 620, 638, 668, 719) from Korean patients. Each carcinoma cell line had unique modal karyotypic characteristics and showed a variable number of numerical and structural clonal cytogenetic aberrations. SNU-484, SNU-620, and SNU-668 had near-triploidy; SNU-601, SNU-638, and SNU-719 had near-diploidy. The origins of the marker chromosomes of these cell lines were identified by fluorescence in situ hybridization with constructed painting probes. In all of six cell lines, rearrangement of chromosome 17 resulting in partial deletion of 17p (and/or partial duplication of 17q) was found. The most frequent marker was a partial gain of chromosome 7 with the breakpoints on 7q22 and 7q31. The nonrandom rearrangements of chromosomes were also determined on 1q32, 5q11-q22, 8q, 14q22, 14q34, and 15q15; suggesting that they may be the candidate regions for the isolation of the genes related to gastric cancer.

Genomic imbalances in Korean hepatocellular carcinoma

Hepatocellular carcinoma (HCC) is one of the most prevalent gastrointestinal malignant tumors in Southeast Asia. Thirty-one cirrhotic HCC, 14 noncirrhotic HCC, and 13 metastastic HCC in the Korean population were investigated on microdissected tissues for chromosomal aberrations by degenerate oligonucleotide-primed polymerase chain reaction (PCR) comparative genomic hybridization. A number of prominent sites of genomic imbalances were observed. The gains of 1q, 6p, 7, 8q, 12q, 13q3-q32, 16p, 17q, and 20q and the losses of 1p, 4q, 6q, 8p, 9p, and 13q regions were observed with a similar high frequency in all types. Various chromosomal aberrations were observed preferentially to specific types. Gains of 4p15-pter, 10q24-qter, 18p11-pter, and 19p10-pter and a loss of 11q14-q22 were observed in the cirrhotic HCC, whereas losses of 14q21-q23 and 10q22-q23 were observed in noncirrhotic HCC. In metastatic HCC, gains of 3q25-qter and Xp21-pter and losses of 21q11-qter and Y were observed. The recurrent gains and losses of chromosomal regions identified in this study are consistent with several previous observations and provide possible candidate regions for the involvement of tumorigenesis and progressions of HCC.

Chromosomal aberrations in neuroblastoma cell lines identified by cross species color banding and chromosome painting

We have studied cytogenetic rearrangements in karyotypes of five neuroblastoma cell lines [SK-N-AS, SK-N-SH, SH-SY5Y, SK-N-MC, SMS-KCNR] by G-banding, cross species color banding (RxFISH), and fluorescence in situ hybridization (FISH) with chromosome painting probes. Each neuroblastoma cell line had unique modal karyotypic characteristics and showed a variable number of numerical and structural clonal cytogenetic aberrations. The number of rearranged chromosomes in SK-N-AS, SK-N-SH, SH-SY5Y, SK-N-MC, and SMS-KCNR was 11, 3, 7, 14 (tetraploid, 20-21), and 6, respectively. The origins of abnormal chromosomes were effectively analyzed by RxFISH and FISH with multiple chromosome painting probes. The chromosomal origin of the homogeneously staining region in SH-SY5Y was identified as coamplification of chromosome bands 2p13 and 2p24 by chromosome microdissection and FISH. The non-random rearrangements of chromosomes were determined on 1p34 approximately p36, 6q16 approximately q21, 8q24, 9q34, 11q13 approximately q23, 16q23 approximately q24, 17q21, and 22q31. These results may provide useful information for further molecular characterization of neuroblastoma.

A comprehensive karyotypic analysis on a newly established sarcomatoid hepatocellular carcinoma cell line SH-J1 by comparative genomic hybridization and chromosome painting

We first established a sarcomatoid hepatocellular carcinoma cell line, designated as SH-J1, and applied comparative genomic hybridization and fluorescence in situ hybridization (FISH) with chromosome painting probes for the characterization of the chromosomal rearrangements. In the SH-J1 cell line, the pleomorphic spindle cells were arranged in bundles of interlacing patterns and were positive in immunohistochemical staining with hepatocyte-related markers. By G-banding and FISH, the chromosomal gains were detected at 6p and 17, whereas losses were observed at 3p21-pter, 3q27-qter, 4, 6q, 13pter-q11, 16, 18, 19p13, and Y.

Detection of genetic alterations in Korean ovarian carcinomas by degenerate oligonucleotide primed polymerase chain reaction-comparative genomic hybridization.

Chromosomal aberrations in 22 Koreans with ovarian carcinomas were investigated by degenerate oligonucleotide primed-polymerase chain reaction comparative genomic hybridization. The common sites of copy number increases were 20q (90%), 17q23 approximately qter (86%), 8q22 approximately qter (68%), 3q25 approximately qter (59%), 6p21 (59%), 11q13 (54%), 16p (40%), 2q31 approximately qter (36%), 7q (36%), 14q31 (36%), 15q24 approximately qter (36%), and 1q32 approximately qter (31%). DNA amplification was identified in 18 carcinomas (82%). The frequent sites of amplification were 20q13.2 approximately qter, 8q24.1, 17q23 approximately qter, 3q25 approximately qter, and 6p21. The most frequent sites of copy number decreases were 4q21 approximately q31 (54%), 5q13 approximately q21 (50%), and 13q14 approximately q21 (45%). The recurrent gains and losses of chromosomal regions identified in this study provide candidate regions that may contain oncogenes or tumor suppressor genes, respectively.