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. Author manuscript; available in PMC: 2012 Jul 1.
Published in final edited form as: Cancer Res. 2011 May 9;71(13):4494–4505. doi: 10.1158/0008-5472.CAN-10-2668

Figure 2. Targeted inhibition of irreversible EGFR-TKI-sensitive H1975 lung adenocarcinoma cells also results in “early' emergence of tumor resistant escape survivor cells with activated prosurvival-antiapoptotic signaling.

Figure 2

A, Significant resistant shift of cell viability in H1975 cells that survived 9 days of CL-387,785 treatment. B, Activation of p-STAT3[Y705]/BCL-2/BCL-XL signaling in H1975 cells that survived 9 days of CL-387,785 treatment. C, Reactivated p-EGFR and downstream signaling in Day 9-resistant-survivors H1975 cells against CL-387,785 (1μM) could be inhibited by higher dose of CL-387,785 (5μM) in retreatment, but not p-STAT3 or BCL-2.

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