Expression and amplification of therapeutic target genes in retinoblastoma.

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

Expression and amplification of therapeutic target genes in retinoblastoma.

Standard

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: GRAEF ARCH CLIN EXP, Jahrgang 243, Nr. 2, 2, 2005, S. 156-162.

Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung

Harvard

Bösch, D, Pache, M, Simon, R, Schraml, P, Glatz, K, Mirlacher, M, Flammer, J, Sauter, G & Meyer, P 2005, 'Expression and amplification of therapeutic target genes in retinoblastoma.', GRAEF ARCH CLIN EXP, Jg. 243, Nr. 2, 2, S. 156-162. <http://www.ncbi.nlm.nih.gov/pubmed/15549365?dopt=Citation>

APA

Bösch, D., Pache, M., Simon, R., Schraml, P., Glatz, K., Mirlacher, M., Flammer, J., Sauter, G., & Meyer, P. (2005). Expression and amplification of therapeutic target genes in retinoblastoma. GRAEF ARCH CLIN EXP, 243(2), 156-162. [2]. http://www.ncbi.nlm.nih.gov/pubmed/15549365?dopt=Citation

Vancouver

Bösch D, Pache M, Simon R, Schraml P, Glatz K, Mirlacher M et al. Expression and amplification of therapeutic target genes in retinoblastoma. GRAEF ARCH CLIN EXP. 2005;243(2):156-162. 2.

Bibtex

@article{a3626f2dcb3a4f4a98f92ff97ee7f924,

title = "Expression and amplification of therapeutic target genes in retinoblastoma.",

abstract = "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.",

author = "Doris B{\"o}sch and Mona Pache and Ronald Simon and Peter Schraml and Katharina Glatz and Martina Mirlacher and Josef Flammer and Guido Sauter and Peter Meyer",

year = "2005",

language = "Deutsch",

volume = "243",

pages = "156--162",

journal = "GRAEF ARCH CLIN EXP",

issn = "0721-832X",

publisher = "Springer",

number = "2",

}

RIS

TY - JOUR

T1 - Expression and amplification of therapeutic target genes in retinoblastoma.

AU - Bösch, Doris

AU - Pache, Mona

AU - Simon, Ronald

AU - Schraml, Peter

AU - Glatz, Katharina

AU - Mirlacher, Martina

AU - Flammer, Josef

AU - Sauter, Guido

AU - Meyer, Peter

PY - 2005

Y1 - 2005

N2 - 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.

AB - 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.

M3 - SCORING: Zeitschriftenaufsatz

VL - 243

SP - 156

EP - 162

JO - GRAEF ARCH CLIN EXP

JF - GRAEF ARCH CLIN EXP

SN - 0721-832X

IS - 2

M1 - 2

ER -