Fig. 7

FAM167A and surface DSG1 levels are associated with BCR-ABL-independent TKI resistance in CML patients. A qRT-PCR analysis of FAM167A mRNA expression in CD34⁺ stem/progenitor cells from imatinib-responsive CML patients (S) at the time of diagnosis (n = 26) and at follow-up (n = 26), in imatinib-resistant CML patients (R) without BCR-ABL mutation at the time of diagnosis (n = 12) and at follow-up (n = 11), and in imatinib-resistant CML patients harboring a BCR-ABL mutation at the time of diagnosis (n = 10) and at follow-up (n = 12). Imatinib resistance and BCR-ABL mutation status were determined at follow-up. The level of FAM167A was normalized to that of GAPDH. B Relative surface expression of DSG1 (MFI) in CD34⁺ stem/progenitor cells from imatinib-responsive CML patients at the time of diagnosis (n = 8) and at follow-up (n = 8), and from imatinib-resistant CML patients without BCR-ABL mutation at the time of diagnosis (n = 10) and at follow-up (n = 7), as measured via flow cytometry. C Proposed model showing involvement of the FAM167A-induced noncanonical NF-κB pathway in BCR-ABL-independent TKI resistance. Unpaired two-tailed t-test; *P < 0.05, ***P < 0.001. NS, not significant