Fig 2: Overall survival time of TNK2 protein expression in 184 esophageal cancer samples (n = 46, high expression; n = 138, low/medium expression. Log‐rank, p = 0.37 of no significance in TNK2 high expression VS TNK2 low/medium expression

Fig 3: (A) Western blot analysis of proteins TNK2, CDC42, Akt, and EGFR. All proteins were increased in esophageal cancer tissues compared to adjacent tissue. (B) TNK2 in poorly differentiated esophageal cancer VS para-carcinoma tissue (&p < 0.05), VS well-differentiated esophageal cancer and moderately differentiated esophageal cancer (#p < 0.05). CDC42 in poorly differentiated esophageal cancer VS para-carcinoma tissue (**p < 0.05). Akt in esophageal cancer tissues VS para-carcinoma tissues (***p < 0.05). Results were means ± SD for six tissue samples in each group, and p < 0.05 was of significance

Fig 4: LCK and ACK1 signaling pathways drive resistance to BH3 mimetics in T-ALL. (Created with BioRender.com.)

Fig 5: ACK1 drives resistance to BCL-2 and BCL-xL inhibition in T-ALL. A, Immunoblots showing ACK1 knockdown (KD) in MOLT4 T-ALL cell line. B, Curves showing viability of MOLT4 NT control and ACK1 KD cells treated with BH3 mimetics. C, BIM titration assay for MOLT4 NT control and ACK1 KD cells. D, BH3 profiling of MOLT4 NT control and ACK1 KD cells. E and F, Immunoblots showing AKT pathway activity and BAD phosphorylation in NWP-R, ACK1 KD, and ACK1 overexpressing (OE) cells, compared with their respective controls. G, Curves showing viability of ALL-SIL empty vector control and ACK1 OE cells treated with BH3 mimetics. H, Immunoblots showing AKT pathway activity and BAD phosphorylation upon capivasertib treatment of ALL-SIL, NWP-R, and MOLT4 cells. I, Immunoblots showing BAD protein pulldown in ALL-SIL control and NWP-R cell lysates, probed with p-BAD, BAD, BCL-2, and BCL-xL (*, P < 0.05; **, P < 0.01; ***, P < 0.001).