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. Author manuscript; available in PMC: 2016 Sep 1.
Published in final edited form as: Clin Cancer Res. 2015 May 26;21(17):3995–4003. doi: 10.1158/1078-0432.CCR-14-2728

Figure 1. Expression of ER and its downstream gene products Bcl2 and PR increases at the time of acquired resistance to HER2-targeting therapy in two different HER2+/ER+ pre-clinical models in vivo.

Figure 1

A. Expression levels of ER, Bcl2, and PR in UACC812 tumor xenografts grown only in the presence of estrogen (E2; n=6) and treated with lapatinib in the presence of E2 (E2 + L; n=6). L-treated tumors showed a significant increase in the expression of ER, PR, and Bcl2, compared with tumors treated with vehicle.

B. Expression levels of ER, Bcl2, and PR in MCF7 HER2-18 tumor xenografts grown in presence of E2 with (n=9) or without (n=9) HER2-targeted therapy. Tumors treated with lapatinib plus trastuzumab (LT) were harvested either when still sensitive to the treatment (n=4) or at the time of acquired resistance (n=5)(8). LT-sensitive tumors showed a non-significant trend toward increase in ER expression, as well as in Bcl2 and PR levels, compared with control tumors (E2). LT-resistant tumors showed a significant increase in ER, Bcl2, and PR expression compared with control.