Fig. 2
From: The importance of personalized medicine in chronic myeloid leukemia management: a narrative review
BCR-ABL-dependent mechanisms, in addition to mutations within the BCR-ABL gene and other proteins, combined mutations, and polymorphisms, overexpression of the BCR-ABL protein, and genomic instability are all contributing factors to this mechanism. Abbreviation SH2, Src homology 2; SH3, Src homology 3; Cap, cysteine-rich secretory proteins; antigen 5; and pathogenesis-related 1 proteins; IRF1, Interferon regulatory factor 1; ALPK2, Alpha Protein Kinase 2; and CYP1B1, cytochrome P450 1B1; ACA, additional chromosomal aberrations; DDR, DNA damage response deregulation