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. Author manuscript; available in PMC: 2015 Mar 1.
Published in final edited form as: Cancer Discov. 2014 Jul 31;4(9):1022–1035. doi: 10.1158/2159-8290.CD-14-0098

Figure 3. Concurrent inactivation of BTKWT and AKT by ibrutnib in responding patients and AKT activation independent of BTKWT inactivation in ibrutinib resistant patients.

Figure 3

A, B, immunoblotting of indicated proteins in MCL cells isolated from responding Pt 4 before (Pt 4 p_Ib1) and on 21 day of ibrutinib treatment (Pt 4_Ib1), Pt 8 on 21 day of ibrutinib treatment (Pt 8 Ib_1), primary resistant Pt 6 and Pt 9 on 21 day of ibrutinib treatment, Pt 5 and Pt 3 before ibrutinib treatment (Pt 5 p_Ib1, Pt 3 p_Ib1), on day 21 (Pt 5 Ib1, Pt 3 Ib1) of ibrutinib treatment and at relapse (Pt 3 r_Ib) after 3 months of ibrutinib response (See Supplementary Table S5 for details). N.S. denotes a non-specific signal. C, immunoblotting of MCL cells from serial lymph node biopsies of Pt 1 before ibrutinib treatment (p_Ib1, p_Ib2) and from the bone marrow at relapse from ibrutinib (r_IbBM). CD19+ B cells isolated from peripheral blood of healthy donors (PBCs) and JEKO-1 cells were used as controls. D, WTS analysis of mRNA abundance (RPKM) of indicated genes serial biopsies of Pt 1 and PBCs, as shown in Figure 1.