Skip to main content
. 2016 Apr 7;1(4):e86082. doi: 10.1172/jci.insight.86082

Figure 1. Focal adhesion kinase pathway upregulation in BCR-ABL1 B progenitor acute lymphoblastic leukemia, with further upregulation by IKZF1 alteration.

Figure 1

(A) Gene expression profiling, (B) mRNA sequencing, and (C) protein sequencing of focal adhesion kinase 1 (Fak1) and Fak2 in murine Arf–/– pre-B cells. (D) mRNA sequencing of human BCR-ABL1+ (Ph+) and Ph-like patient cohorts. (E) Reverse-phase protein array (RPPA) analysis of FAK1 expression and downstream targets of FAK signaling in human Ph+ B progenitor acute lymphoblastic leukemia (B-ALL) (h9407) cells with and without IKZF1 alteration (IK6). Data represent averages ± SD; n = 5 technical replicates each in A, 3 (MIG) and 4 (IK6) biological replicates in B, 3 biological replicates in C, 19 Ph+ and 109 Ph-like patients in D, and 4 technical replicates of 2 biological replicates in D. *P ≤ 0.05, **P ≤ 0.005, ***P ≤ 0.0005, 2-tailed Student’s t test. MIG, MSCV-IRES-GFP (empty GFP vector); FPKM, fragments per kilobase of transcripts per million mapped reads.