fig1

Figure 1. Genomic landscape and molecular pathogenesis of chronic myeloid leukemia. The primary molecular driver, the BCR::ABL1 fusion gene, originates from the reciprocal translocation between chromosomes 9 and 22 [t(9;22)(q34;q11)], resulting in the formation of the characteristic Philadelphia chromosome (Ph). This genomic aberration leads to constitutive activation of tyrosine kinase signaling, which serves as the foundational event in CML pathogenesis. The hollow circles on the orange chromosome schematically indicate chromosomal banding and reference loci used to orient the reader, rather than independent genes or mutations. This figure was redrawn by the authors using Python-based vector drawing and Microsoft Office-compatible elements; no third-party copyrighted materials were reused. CML: Chronic myeloid leukemia; Ph: philadelphia chromosome; LSC: leukemia stem cell.