Al materialAdditional file 1: Supplemental tables and figures. Supplemental Table S1: Oligonucleotides applied for quantitative RT-PCR to validate expression from the chosen from microarray study. Supplemental Table S2: List of your antibodies applied for western blot. Supplemental Table S3: Topten pathways more associated to resistance to 17AAG. Supplemental Figure S1: Unsupervised clustering showed that samples mainly grouped by cell line. Some samples have technical Glutarylcarnitine manufacturer replicates (marked using a star). Supplemental Figure S2: QT-PCR measurements of selected genes from the signature, confirmed the down regulation of five genes from the molecular signature (CYCLIN D1, JUNB, TMEM129, PLK3, NFKBIA) and upregulation of UBE2C immediately after treatment.List of abbreviations 17AAG: 17-allyloamino-17-demethoxy-geldanamycin; DMSO: Dimethyl sulfoxide; FDR: False Discovery Rate; GSEA: Gene Set Enrichment Analysis; QT-PCR: Quantitative real-time Polymerase Chain Reaction. Competing interests The authors declare that they have no competing interests. Authors’ Ethyl glucuronide Metabolic Enzyme/Protease contributions MZ carried out hybridizations, participated inside the evaluation of outcomes and happen to be involved in drafting the manuscript. GG gave help for the analysis and interpretation of microarray data and performed the statistical evaluation. JB participated within the design from the study and analysis of results. BMD conception and design with the study, supervision of experiments and helped to draft the manuscript. All authors study and authorized the final manuscript. Acknowledgements This perform was supported by grants from Spanish Fondo de Investigaciones Sanitarias (FIS-PI081298) and Grant from Ministerio de Education y Ciencia (MEC), SAF06-06140.Author facts Human Genetics Group, Spanish National cancer Centre (CNIO), Madrid, Spain. 2Bioinformatics Unit. CNIO, Madrid, Spain. 3CIBERER, Centre for Biomedical Networking Investigation on Rare diseases, Madrid, Spain. Received: 11 Might 2010 Accepted: 4 October 2010 Published: four OctoberReferences 1. Eccles SA, Massey A, Raynaud FI, Sharp SY, Box G, Valenti M, Patterson L, de Haven Brandon A, Gowan S, Boxall F, et al: NVP-AUY922: a novel heat shock protein 90 inhibitor active against xenograft tumor development, angiogenesis, and metastasis. Cancer Res 2008, 68(eight):2850-2860. 2. Chiosis G, Timaul MN, Lucas B, Munster PN, Zheng FF, Sepp-Lorenzino L, Rosen N: A small molecule designed to bind towards the adenine nucleotide pocket of Hsp90 causes Her2 degradation and the growth arrest and differentiation of breast cancer cells. Chem Biol 2001, 8(3):289-299. 3. Neckers L: Heat shock protein 90 inhibition by 17-allylamino-17demethoxygeldanamycin: a novel therapeutic approach for treating hormone-refractory prostate cancer. Clin Cancer Res 2002, eight(five):962-966. 4. Modi S, Stopeck AT, Gordon MS, Mendelson D, Solit DB, Bagatell R, Ma W, Wheler J, Rosen N, Norton L, et al: Combination of trastuzumab and tanespimycin (17-AAG, KOS-953) is protected and active in trastuzumabrefractory HER-2 overexpressing breast cancer: a phase I dose-escalation study. J Clin Oncol 2007, 25(34):5410-5417. 5. Caldas-Lopes E, Cerchietti L, Ahn JH, Clement CC, Robles AI, Rodina A, Moulick K, Taldone T, Gozman A, Guo Y, et al: Hsp90 inhibitor PU-H71, a multimodal inhibitor of malignancy, induces full responses in triple-negative breast cancer models. Proc Natl Acad Sci USA 2009, 106(20):8368-8373. 6. Bao R, Lai CJ, Qu H, Wang D, Yin L, Zifcak B, Atoyan R, Wang J, Samson M, Forrester J, et al: CUDC-305, a novel synthetic.