Chromosomal imbalances in Korean intrahepatic cholangiocarcinoma by comparative genomic hybridization

Kyung Ok Uhm; Young Nyun Park; Ji Young Lee; Dong Seop Yoon; Sun Hwa Park

doi:10.1016/j.cancergencyto.2004.05.007

Chromosomal imbalances in Korean intrahepatic cholangiocarcinoma by comparative genomic hybridization

Kyung Ok Uhm, Young Nyun Park, Ji Young Lee, Dong Seop Yoon, Sun Hwa Park

Research output: Contribution to journal › Article

23 Citations (Scopus)

Abstract

Intrahepatic cholangiocarcinoma (ICC) arises from epithelial cells in the intrahepatic bile duct. Until now, only few reports have been available concerning the genetic changes during the progression of ICC. In this study, we analyzed chromosomal aberrations in 19 frozen ICC samples using comparative genomic hybridization. The common chromosomal gains were observed in 8q22∼qter (11 cases, 58%), 5p14∼pter (32%), 2q33∼qter (26%), 7p (26%), 17q21∼q22 (26%), 18q12∼q21 (26%), and 19q13.1 (26%). DNA amplification was identified in nine tumors (47%). Chromosomal loss was found in Y (60%), 1p34∼pter (37%), 4q(32%), 18q21∼qter (32%) 19p (32%), X (32%), 5q11∼q14 (26%), 8p(26%), 9p (26%), and 17p (26%). Chromosomal aberrations identified in this study provide candidate regions involved in the tumorigenesis and progression of ICC.

Original language	English
Pages (from-to)	37-41
Number of pages	5
Journal	Cancer Genetics and Cytogenetics
Volume	157
Issue number	1
DOIs	https://doi.org/10.1016/j.cancergencyto.2004.05.007
Publication status	Published - 2005 Feb
Externally published	Yes

ASJC Scopus subject areas

Molecular Biology
Genetics
Cancer Research

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Uhm, K. O., Park, Y. N., Lee, J. Y., Yoon, D. S., & Park, S. H. (2005). Chromosomal imbalances in Korean intrahepatic cholangiocarcinoma by comparative genomic hybridization. Cancer Genetics and Cytogenetics, 157(1), 37-41. https://doi.org/10.1016/j.cancergencyto.2004.05.007

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abstract = "Intrahepatic cholangiocarcinoma (ICC) arises from epithelial cells in the intrahepatic bile duct. Until now, only few reports have been available concerning the genetic changes during the progression of ICC. In this study, we analyzed chromosomal aberrations in 19 frozen ICC samples using comparative genomic hybridization. The common chromosomal gains were observed in 8q22∼qter (11 cases, 58%), 5p14∼pter (32%), 2q33∼qter (26%), 7p (26%), 17q21∼q22 (26%), 18q12∼q21 (26%), and 19q13.1 (26%). DNA amplification was identified in nine tumors (47%). Chromosomal loss was found in Y (60%), 1p34∼pter (37%), 4q(32%), 18q21∼qter (32%) 19p (32%), X (32%), 5q11∼q14 (26%), 8p(26%), 9p (26%), and 17p (26%). Chromosomal aberrations identified in this study provide candidate regions involved in the tumorigenesis and progression of ICC.",

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AU - Park, Sun Hwa

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N2 - Intrahepatic cholangiocarcinoma (ICC) arises from epithelial cells in the intrahepatic bile duct. Until now, only few reports have been available concerning the genetic changes during the progression of ICC. In this study, we analyzed chromosomal aberrations in 19 frozen ICC samples using comparative genomic hybridization. The common chromosomal gains were observed in 8q22∼qter (11 cases, 58%), 5p14∼pter (32%), 2q33∼qter (26%), 7p (26%), 17q21∼q22 (26%), 18q12∼q21 (26%), and 19q13.1 (26%). DNA amplification was identified in nine tumors (47%). Chromosomal loss was found in Y (60%), 1p34∼pter (37%), 4q(32%), 18q21∼qter (32%) 19p (32%), X (32%), 5q11∼q14 (26%), 8p(26%), 9p (26%), and 17p (26%). Chromosomal aberrations identified in this study provide candidate regions involved in the tumorigenesis and progression of ICC.

AB - Intrahepatic cholangiocarcinoma (ICC) arises from epithelial cells in the intrahepatic bile duct. Until now, only few reports have been available concerning the genetic changes during the progression of ICC. In this study, we analyzed chromosomal aberrations in 19 frozen ICC samples using comparative genomic hybridization. The common chromosomal gains were observed in 8q22∼qter (11 cases, 58%), 5p14∼pter (32%), 2q33∼qter (26%), 7p (26%), 17q21∼q22 (26%), 18q12∼q21 (26%), and 19q13.1 (26%). DNA amplification was identified in nine tumors (47%). Chromosomal loss was found in Y (60%), 1p34∼pter (37%), 4q(32%), 18q21∼qter (32%) 19p (32%), X (32%), 5q11∼q14 (26%), 8p(26%), 9p (26%), and 17p (26%). Chromosomal aberrations identified in this study provide candidate regions involved in the tumorigenesis and progression of ICC.

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