May 2003
Volume 44, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2003
Effects of 13-cis Retinoic Acid in Human Retinoblastoma Cell Lines
Author Affiliations & Notes
  • C.T. Tong
    Dept. of Ophthalmology, University of California San Francisco, San Francisco, CA, United States
  • K.R. Van Quill
    Dept. of Ophthalmology, University of California San Francisco, San Francisco, CA, United States
  • N.A. Sharara
    Dept. of Ophthalmology, University of California San Francisco, San Francisco, CA, United States
  • A. Gupta
    Dept. of Ophthalmology, University of California San Francisco, San Francisco, CA, United States
  • J.M. O'Brien
    Dept. of Ophthalmology, University of California San Francisco, San Francisco, CA, United States
  • Footnotes
    Commercial Relationships  C.T. Tong, None; K.R. Van Quill, None; N.A. Sharara, None; A. Gupta, None; J.M. O'Brien, None.
  • Footnotes
    Support  Research to Prevent Blindness Physician-Scientist Award, Sandhill Foundation, and NEI Grant EY13812
Investigative Ophthalmology & Visual Science May 2003, Vol.44, 1579. doi:
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    • Get Citation

      C.T. Tong, K.R. Van Quill, N.A. Sharara, A. Gupta, J.M. O'Brien; Effects of 13-cis Retinoic Acid in Human Retinoblastoma Cell Lines . Invest. Ophthalmol. Vis. Sci. 2003;44(13):1579.

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

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Abstract

Abstract: : Purpose: 13-cis retinoic acid (13-CRA) has demonstrated anticancer effects in animal tumor models and clinically in patients with several malignancies. In this study we evaluated the potential utility of 13-CRA in the treatment of retinoblastoma. Methods: Dose-dependent antiproliferative effects of 13-CRA were investigated in Y79 and Weri-RB1 human retinoblastoma cell lines. Cells were treated with 13-CRA at concentrations ranging from 0.1 to 20 µM. At 96 hours post-treatment, antiproliferative effects were determined by WST-1 Cell Proliferation Assay (Roche) and Cell Titer-Glo Luminescent Cell Viability Assay (Promega). All assays were performed in triplicate. Criterion for a positive result was induction of 50% growth inhibition (IC50) within clinically achievable plasma levels (< 7.4 µM). Results: Within clinically achievable levels, 13-CRA inhibited proliferation of Y79 and Weri-RB1 cells by a maximum of 41% and 43%, respectively. However, even at higher concentrations this agent failed to induce 50% growth inhibition in either cell line. Conclusions: 13-CRA mildly inhibited retinoblastoma cell growth in vitro at clinically relevant concentrations. These results suggest that this agent may be useful as an adjuvant therapy in clinical management of retinoblastoma.

Keywords: retinoblastoma • oncology • tumors 
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