Immature CML cells implement a BMP autocrine loop to escape TKI treatment

Chronic myeloid leukemia (CML) is a clonal myeloproliferative disorder emanating from a reciprocal translocation between BCR on chromosome 22 and ABL kinase on chromosome 9, generally known as the Philadelphia chromosome. Although activity level of ABL kinase in the resting condition is preserved and regulated by a hydrophobic pocket, in CML, this pocket substitute with BCR that engenders in incessant activation of ABL and culminates in actuation of downstream signaling pathways (1,2).