Article Title: AKT-aro and HER2-aro, models for de novo resistance to aromatase inhibitors; molecular characterization and inhibitor response studies Journal Name: Breast Cancer Research and Treatment Author Names and Affiliations: Cynthie Wong 1, Xin Wang 1, David Smith 2, Kaladhar Reddy 3 and Shiuan Chen 1 1 Division of Tumor Cell Biology, 2 Department of Information Sciences, Beckman Research Institute of the City of Hope, Duarte, CA 91010, 3 Department of Pathology, Wayne State University, Detroit, MI Corresponding author address:

Supplementary Table 1; Wong, Wang, Smith, Reddy and Chen Kinetic analysis of aromatase activity Cell lineV max (nmol/mg/h)K m (nM) MCF-7aro16.97 ± ± 1.28 AKT-aro5.4 ± ± 2.24 HER2-aro9.72 ± ± 6.39 Aromatase kinetic analysis was carried out in triplicate. Mean ± SD are shown.

24 hr 48 hr72 hr Supplementary Figure 1; Wong, Wang, Smith, Reddy and Chen A B 24 hr 48 hr 72 hr Supplementary Figure DMAG induces G 2 phase arrest. Cells were treated with either DMSO or 100 nM 17-DMAG for 24, 48, or 72 h. a) AKT-aro and b) HER2-aro cells were stained with propidium iodide and analyzed by flow cytometry. AKT-aroHER2-aro

Supplementary Figure 2; Wong, Wang, Smith, Reddy and Chen Supplementary Figure DMAG suppresses ER activity. The pGL3-(ERE) 3 reporter plasmid was transiently transfected into MCF-7aro, AKT-aro and HER2-aro cell lines. Cell lines were treated with either DMSO or 100 nM 17- DMAG, in addition to 1 nM E 2 for 48 hours. Data (mean ± SD) is representative of 3 independent experiments performed in triplicate.