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- W2009797653 abstract "Triple negative breast cancers (TNBCs) have a relatively poor prognosis emphasising the need to identify new subtype specific target therapies. Based on the concept of oncogene addiction, we searched for potential therapeutic targets by identifying genes consistently over-expressed when amplified in TNBC. Fifty six TNBCs were subjected to high resolution tiling path microarray-based comparative genomic hybridisation (aCGH); out of these cases, 24 were also subjected to genome-wide microarray-based mRNA expression analysis. TNBCs showed a high level of genetic instability, with recurrent regions of amplification (>4 copies) included multiple regions on 1q and 8q, 3q25, 10p14, 10q26, 13q34, 15q26 and 19q12-19q13. Integration of aCGH and expression data revealed 38 genes that were significantly overexpressed when amplified. This list includes known oncogenes and potential therapeutic targets, such as MCL1 (1q21.2), FGFR2 (10q26.3), BUB3 (10q26.3), RAB20 (13q34),PKN1 (19p13.12), and NOTCH3 (19p13.12). To validate FGFR2 as a therapeutic target, we screened a panel of cell lines, by western blotting and aCGH, and identified two TNBC cell lines with FGFR2 amplification. In these cell lines FGFR2 was constitutively active in a ligand independent manner, and RNA interference-mediated silencing of FGFR2 selectively decreased survival of cell lines harbouring FGFR2 amplification. Likewise FGFR2 amplified cell lines were highly sensitive to FGFR tyrosine kinase inhibitor PD173074 (IC50 Citation Information: Cancer Res 2009;69(24 Suppl):Abstract nr 3147." @default.
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- W2009797653 date "2009-12-15" @default.
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- W2009797653 title "Integrative Molecular Profiling of Triple Negative Breast Cancers Identifies Potential Therapeutic Targets Including Amplifications of FGFR2." @default.
- W2009797653 doi "https://doi.org/10.1158/0008-5472.sabcs-09-3147" @default.
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