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Expression and amplification of therapeutic target genes in retinoblastoma

Bösch, Doris ; Pache, Mona ; Simon, Ronald ; Schraml, Peter ; Glatz, Katharina ; Mirlacher, Martina ; Flammer, Josef ; Sauter, Guido ; Meyer, Peter

In: Graefe's Archive for Clinical and Experimental Ophthalmology, 2005, vol. 243, no. 2, p. 156-162

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    Titre
    • Expression and amplification of therapeutic target genes in retinoblastoma
    Auteur
    • Bösch, Doris. Universitäts-Augenklinik Basel, Mittlere Strasse 91, 4056, Basel, Switzerland
    • Pache, Mona. Universitäts-Augenklinik Basel, Mittlere Strasse 91, 4056, Basel, Switzerland
    • Simon, Ronald. Institut für Pathologie, Universität Basel, Basel, Switzerland
    • Schraml, Peter. Institut für Pathologie, Universität Basel, Basel, Switzerland
    • Glatz, Katharina. Institut für Pathologie, Universität Basel, Basel, Switzerland
    • Mirlacher, Martina. Institut für Pathologie, Universität Basel, Basel, Switzerland
    • Flammer, Josef. Universitäts-Augenklinik Basel, Mittlere Strasse 91, 4056, Basel, Switzerland
    • Sauter, Guido. Institut für Pathologie, Universität Basel, Basel, Switzerland
    • Meyer, Peter. Universitäts-Augenklinik Basel, Mittlere Strasse 91, 4056, Basel, Switzerland
    Type de document
    • Postprint
    Langue
    • Inglese
    Publié dans
    • Graefe's Archive for Clinical and Experimental Ophthalmology, 2005, vol. 243, no. 2, p. 156-162. Springer-Verlag; http://www.springer.de
    Autre version électronique
    Classification
    • Santé
    Identifiant OAI-PMH
    • oai:doc.rero.ch:317853
    Summary
    Purpose: We set out to evaluate alterations of the therapeutic target genes KIT (CD 117), EGFR, and HER-2 in human retinoblastoma. Methods: Ninety-five formalin-fixed, paraffin-embedded retinoblastomas were brought into a tissue microarray (TMA) format. Immunohistochemistry was performed to analyze the expression of CD117, EGFR, and HER-2. Fluorescence in situ hybridization (FISH) was utilized for detection of EGFR amplifications. Three tumors with strong CD117 positivity were sequenced for KIT exon 11 mutations. Results: Detectable CD117 expression was seen in 19% of all interpretable cases. Sequence analysis of the three tumors with the strongest CD117 expression revealed no mutations. EGFR was positive in 14% of all cases. No EGFR amplification was observed by FISH, however. All tumors were negative for HER-2 expression. Conclusions: Our data suggest that selected cases of retinoblastoma may be candidates for anti-EGFR and imatinib mesylate (STI571) therapy