May 2005
Volume 46, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2005
Expression of p53–Induced Apoptosis Effector in Uveal Melanoma With Different Cytogenetical Characteristics
Author Affiliations & Notes
  • L.I. Paraoan
    School of Clinical Sciences, Unit of Ophthalmology, University of Liverpool, Liverpool, United Kingdom
  • D. Gray
    School of Clinical Sciences, Unit of Ophthalmology, University of Liverpool, Liverpool, United Kingdom
  • P. Hiscott
    School of Clinical Sciences, Unit of Ophthalmology, University of Liverpool, Liverpool, United Kingdom
  • I. Grierson
    School of Clinical Sciences, Unit of Ophthalmology, University of Liverpool, Liverpool, United Kingdom
  • B. Damato
    Ocular Oncology Centre, St. Paul's Eye Unit, Royal Liverpool University Hospital, Liverpool, United Kingdom
  • Footnotes
    Commercial Relationships  L.I. Paraoan, None; D. Gray, None; P. Hiscott, None; I. Grierson, None; B. Damato, None.
  • Footnotes
    Support  North West Cancer Research Fund and University of Liverpool Research and Development Fund
Investigative Ophthalmology & Visual Science May 2005, Vol.46, 3411. doi:
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      L.I. Paraoan, D. Gray, P. Hiscott, I. Grierson, B. Damato; Expression of p53–Induced Apoptosis Effector in Uveal Melanoma With Different Cytogenetical Characteristics . Invest. Ophthalmol. Vis. Sci. 2005;46(13):3411.

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

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Abstract

Abstract: : Purpose: To characterize the expression of the p53 apoptosis effector PERP, identified by microarray–based profiling as a putative molecular determinant of aggressiveness in choroidal melanoma, in relation to cytogenetical characteristics of these tumors. Methods: Transcriptional level of PERP gene was quantitated by real–time RT–PCR using SYBR–Green incorporation in choroidal melanoma specimens with known chromosome 3 and 8 cytogenetical characteristics. Gene–specific primers and a probe of 120 bp were used for quantification. Amplification in similar conditions of a non–changing gene was performed as a normalizing control. Protein level was assessed with a polyclonal anti–PERP antibody by Western blotting of tumor lysates and immunohistochemistry, using standard protocols. Results: PERP immunoreactivity of varying intensities was detected in paraffin–embedded tumor specimens, with a uniform distribution in both spindle and epithelioid–type tumor cells and in some endothelial cells in the tumor. PERP mRNA level appeared significantly downregulated in monosomy 3 tumors compared with the level detected in disomy 3 tumors. Furthermore, Western blot analysis of tumor homogenates indicated a reduced level of the 21kDa form of the PERP protein in monosomy 3 versus disomy 3 choroidal melanomas. Conclusions: Our findings suggest that PERP, a p53 target gene, may play a role in uveal melanoma pathogenesis and that its downregulation/loss of function is particularly relevant to the aggressive type of this tumor by specifically impairing apoptosis and thus promoting tumor progression.

Keywords: apoptosis/cell death • melanoma • gene/expression 
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