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Acute myeloid leukemia (AML) is associated with poor clinical outcome and the development of more effective therapies is urgently needed. G protein-coupled receptors (GPCRs) represent attractive therapeutic targets, accounting for approximately 30% of all targets of marketed drugs. Using next-generation sequencing, we studied the expression of 772 GPCRs in 148 genetically diverse AML specimens, normal blood and bone marrow cell populations as well as cord blood-derived CD34-positive cells. Among these receptors, 30 are overexpressed and 19 are downregulated in AML samples compared with normal CD34-positive cells. Upregulated GPCRs are enriched in chemokine ( CCR1 ,  CXCR4 ,  CCR2 ,  CX3CR1 ,  CCR7  and  CCRL2 ), adhesion ( CD97 ,  EMR1 ,  EMR2  and  GPR114 ) and purine (including  P2RY2  and  P2RY13 ) receptor subfamilies. The downregulated receptors include adhesion GPCRs, such as  LPHN1 ,  GPR125 ,  GPR56 ,  CELSR3  and  GPR126 , protease-activated receptors ( F2R  and  F2RL1 ) and the Frizzled family receptors  SMO  and  FZD6 . Interestingly, specific deregulation was observed in genetically distinct subgroups of AML, thereby identifying different potential therapeutic targets in these frequent AML subgroups.

blood cancer journal

Transcriptome analysis of G protein-coupled receptors in distinct genetic subgroups of acute myeloid leukemia: identification of potential disease-specific targets