PATH-10. COPY NUMBER (CN)/SINGLE NUCLEOTIDE POLYMORPHISM (SNP) MICROARRAY ANALYSIS OF THE EGFR LOCUS IN GLIOSARCOMA

• Published in: Neuro-oncology (Charlottesville, Va.) Vol. 20; no. suppl_6; p. vi160
• Main Authors: Lowder, Lindsey, Woods, Ashley, Neill, Stewart, Hauenstein, Jennifer, Debra, Saxe, Weinberg, Brent, Olson, Jeffrey, Shu, Hui-Kuo, Eaton, Bree, Sengupta, Soma
• Format: Journal Article
• Language: English
• Published: US Oxford University Press 05.11.2018
• Subjects: Abstracts
• ISSN: 1522-8517; 1523-5866
• DOI: 10.1093/neuonc/noy148.666

Abstract Epidermal growth factor receptor (EGFR) is overexpressed or mutated in a variety of malignancies, most notably non-small cell lung cancer, colorectal cancer and glioblastoma (GBM). Glioblastoma is an aggressive primary brain tumor and 35–50% of glioblastomas show amplification of the EGFR locus (7p11.2). Interestingly, gliosarcoma, a histologic variant of GBM, has a lower frequency of EGFR alterations (4–8%). We characterized EGFR alterations in gliosarcoma using a DNA copy number/single nucleotide polymorphism cytogenomic microarray using formalin fixed paraffin embedded tissue. A retrospective search for “gliosarcoma” from our database yielded 19 cases on which microarray analysis was performed. Of these cases, 2 showed an amplification at the EGFR locus (13%), 5 cases showed a gain of the entire chromosome 7 (26.3%), 3 cases showed gains at loci other than EGFR (15.8%) and the remaining 9 cases were negative for chromosome 7 alterations (47.4%). Our preliminary data show that amplification of the EGFR locus are infrequent (13%) in gliosarcomas. These preliminary findings demonstrate antithetical results regarding EGFR amplifications in conventional glioblastoma compared to gliosarcoma and suggests there may be an alternate driver in gliosarcoma genesis.