@article {38,
	title = {Modeling ERBB receptor-regulated G1/S transition to find novel targets for de novo trastuzumab resistance},
	journal = {BMC systems biology},
	volume = {3},
	year = {2009},
	month = {2009},
	pages = {1},
	abstract = {In breast cancer, overexpression of the transmembrane tyrosine kinase ERBB2 is an adverse prognostic marker, and occurs in almost 30\% of the patients. For therapeutic intervention, ERBB2 is targeted by monoclonal antibody trastuzumab in adjuvant settings; however, de novo resistance to this antibody is still a serious issue, requiring the identification of additional targets to overcome resistance. In this study, we have combined computational simulations, experimental testing of simulation results, and finally reverse engineering of a protein interaction network to define potential therapeutic strategies for de novo trastuzumab resistant breast cancer.},
	keywords = {Antibodies, Monoclonal, Antibodies, Monoclonal, Humanized, Blotting, Western, Breast Neoplasms, Cell Line, Tumor, Computer Simulation, DNA-Binding Proteins, Drug Delivery Systems, Female, G1 Phase, Humans, Models, Biological, Protein Engineering, Receptor, Epidermal Growth Factor, Reverse Transcriptase Polymerase Chain Reaction, Signal Transduction, Transcription Factors},
	issn = {1752-0509},
	author = {Sahin, Ozg{\"u}r and Fr{\"o}hlich, Holger and L{\"o}bke, Christian and Korf, Ulrike and Burmester, Sara and Majety, Meher and Mattern, Jens and Schupp, Ingo and Chaouiya, Claudine and Thieffry, Denis and Poustka, Annemarie and Wiemann, Stefan and Beissbarth, Tim and Arlt, Dorit}
}
