Development of Chronic Myeloid Leukaemia in Patients Treated with Anti-VEGF Therapies for Clear Cell Renal Cell Cancer

Figures & data

Figure 1. Interaction between environmental factors (DNA damage) and tyrosine kinase inhibitors (sunitinib and sorafenib) in the promotion of chronic myeloid leukemia development.

TKI (So and Su) and kinases inhibited by TKIs (Flt-3, ERCC-1, XRCC-1, PLK4 and CSF-1R). Blue arrows indicate inhibitory activity of TKI on target genes. Yellow arrows indicate promotion of cellular events: cell cycle arrest in G1 phase; DNA repair; NHEJ; and Ph developement. Black arrows indicate inhibition of cellular processes mediated by inhibited TKI: CMP proliferation and differentiation. Red arrows indicate processes leading to CML cells proliferation.

CML: Chronic myeloid leukaemia; CMP: Common myeloid progenitor; NHEJ: Non-homologous end-joining pathway; Ph: Philadelphia chromosome; So: Sorafenib; Su: Sunitinib; TKI: Tyrosine kinase inhibitor.