May 2007
Volume 48, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2007
Comparative Genomic Hybridization Array Analysis of Newly Established Retinoblastoma Cell Lines Compared to Y79
Author Affiliations & Notes
  • Y.-K. Kim
    Ophthalmology, Seoul National University Hospital, Seoul, Republic of Korea
  • Y. S. Yu
    Ophthalmology, Seoul National University Hospital, Seoul, Republic of Korea
  • J. Kim
    Ophthalmology, Seoul National University Hospital, Seoul, Republic of Korea
  • D. Kim
    Radiology, Chosun University Hospital, Kwangju, Republic of Korea
  • J. Kim
    Division of Pharmaceutical Bioscience, College of Pharmacy, Seoul National University, Seoul, Republic of Korea
  • J. Kim
    Division of Pharmaceutical Bioscience, College of Pharmacy, Seoul National University, Seoul, Republic of Korea
  • K.-W. Kim
    Division of Pharmaceutical Bioscience, College of Pharmacy, Seoul National University, Seoul, Republic of Korea
  • Footnotes
    Commercial Relationships Y. Kim, None; Y.S. Yu, None; J. Kim, None; D. Kim, None; J. Kim, None; J. Kim, None; K. Kim, None.
  • Footnotes
    Support None.
Investigative Ophthalmology & Visual Science May 2007, Vol.48, 1586. doi:
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    • Get Citation

      Y.-K. Kim, Y. S. Yu, J. Kim, D. Kim, J. Kim, J. Kim, K.-W. Kim; Comparative Genomic Hybridization Array Analysis of Newly Established Retinoblastoma Cell Lines Compared to Y79. Invest. Ophthalmol. Vis. Sci. 2007;48(13):1586.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Purpose:: To analyze genomic aberration of newly established retinoblastoma cell lines of adherent growth, SNUOT-Rb1 and -Rb4, compared to Y79 cell line of non-adherent growth

Methods:: We used array comparative genomic hybridization (array CGH) in newly established retinoblastoma cell lines SNUOT-Rb1, -Rb4, and Y79 cell line. Copy number gain and loss in chromosomal regions were detected.

Results:: Y79 showed 45 significant chromosomal copy number changes (gain in 41 and loss in 4, P<0.01). SNUOT-Rb1 showed 44 significant copy number changes, (gain in 11 and loss in 33, P<0.01). SNUOT-Rb4 showed 42 significant copy number changes (gain in 8 and loss in 34, P<0.01). The adherent cell line, SNUOT-Rb1 and -RB4 represented similar pattern in gain and loss of chromosomal copy number changes, while different from Y79. The loss of CYLD gene, 16q12-q13, was only one locus of common involvement in three cell lines. Y79 cell line had the greatest gain, 19.65 fold, in the locus of MYCN gene, 2p24.1, where SNUOT-Rb1 and -Rb4 showed no significant gain. Gains of chromosomal copy number in Y79 occurred in chromosome 17, 18, 21. Losses were only in 4 loci, 16q12-q13, 20q tel, Yp11.3, and Yq11. SNUOT-Rb1 and -Rb4 gained chromosomal copy numbers commonly in chromosome 11, especially in locus 11q13 which is responsible for many cancer related genes, CCND1, MEN1, FGF3, FGF4, and EMS1. Losses of copy numbers occurred in chromosome 3, 9, 10, 11, 16, 17.

Conclusions:: SNUOT-Rb1 and -Rb4 of adherent growth showed quite different patterns in chromosomal copy numbers from Y79 cell line of non-adherent growth, but were similar to each other. Loss of 16q12-q13, common in all three may coincide by accident, but 16q12-q13 is related to CYLD gene known as tumor suppressor gene. More studies should be performed to define the detected genomic aberration.

Keywords: retinoblastoma • gene microarray • retina 
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