Table 3.

The role of the non-receptor tyrosine kinase, focal adhesion kinase (FAK), in human AML.

FAK expression is significantly higher in MDS that later transform to AML [66]. FAK expression is detected only for a subset of patients; FAK was then activated at Tyr-397 and this was associated with increased blast migration, increased marrow cellularity and adverse prognosis [67]. High FAK expression is associated with unfavorable cytogenetics and an increased risk of AML relapse, and this expression correlates with integrin β3 expression [68]. FAK splice variants are abnormally expressed in leukemic stem cells from patients with adverse prognosis, and these abnormal variants cause activation of β-catenin and thus replace the Wnt-controlled β-catenin activation [66]. Constitutive activation of FAK activation has an essential role in nuclear translocation of Signal transducer and activator of transcription (STAT5) in AML with FLT3 and KIT mutations [69]. Integrin α4β1 expression, CXC chemokine receptor 4 (CXCR4) expression and FAK activation seem to have additive adverse prognostic impacts [70].