May 2003
Volume 44, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2003
The Potential Clinical Utility of Fenretinide in the Treatment of Retinoblastoma: In Vitro Study
Author Affiliations & Notes
  • N.A. Sharara
    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
  • J.M. O'Brien
    Dept. of Ophthalmology, University of California San Francisco, San Francisco, CA, United States
  • Footnotes
    Commercial Relationships  N.A. Sharara, None; K.R. Van Quill, None; J.M. O'Brien, None.
  • Footnotes
    Support  Knights Templar Eye Foundation, Research to Prevent Blindness, Sandhill Grant, NEI Grant EY13812
Investigative Ophthalmology & Visual Science May 2003, Vol.44, 1581. doi:
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      N.A. Sharara, K.R. Van Quill, J.M. O'Brien; The Potential Clinical Utility of Fenretinide in the Treatment of Retinoblastoma: In Vitro Study . Invest. Ophthalmol. Vis. Sci. 2003;44(13):1581.

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

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Abstract

Abstract: : Purpose: To investigate the potential clinical utility of the synthetic retinoid, N-(4-hydroxyphenyl)retinamide (fenretinide), in the treatment of retinoblastoma. Methods: Dose-dependent antiproliferative effects of fenretinide were investigated in human retinoblastoma cells in vitro. Established retinoblastoma cell lines, Y79 and Weri-RB1, and primary retinoblastoma cells from patient enucleation specimens were treated with fenretinide at a range of concentrations which spanned clinically observed plasma levels. At a 96 hour endpoint, dose-dependent antiproliferative effects were determined by WST-1 Cell Proliferation Assay (Roche) and Cell Titer-Glo ATP Luminescent Cell Viability Assay (Promega). Assays were performed in triplicate. Results were regarded as positive if the concentration required to induce 50% growth inhibition (IC50) fell within clinically achievable plasma levels. Results: At 96 hours post-treatment, the IC50 of fenretinide was approximately 3µM in Y79 and Weri-RB1 cell lines and 6µM in primary cells from retinoblastoma patients. Results were comparable with both WST-1 Cell Proliferation Assay and Cell Titer-Glo ATP Luminescent Cell Viability Assay. Conclusions: Fenretinide inhibits the proliferation of retinoblastoma cells in vitro at clinically achievable concentrations. This agent has potential efficacy in the treatment of retinoblastoma patients.

Keywords: retinoblastoma • oncology • tumors 
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