Fig. 6.

Schematic of molecular alterations and potential therapeutic targets in AML. Accumulation of diverse genomic and transcriptomic aberrations is related to the risk and prognosis of AML. Potential AML-related abnormalities identified in this work are displayed in the cell diagram (cell membrane, cytoplasm, nucleus) including fusion transcripts, genetic mutations, prognostic gene expression and alternative splicing events. Genetic mutations involving activated signaling molecules are common in the cytoplasm and cell membrane. Nuclear regulatory factors may contribute to the instability of the genome resulting in specific genetic mutations and gene expression profiles. Genes with sequence variations are marked with red lightning marks. The known and emerging target therapy agents are also labeled accompanying the target gene or pathway. Venetoclax and Glasdegib are respectively targeting the de-regulated apoptosis pathway gene BCL2 and the Hedgehog pathway SMO. Inhibitors Midostaurin and Gilteritinib can be used to treat FLT3 mutant AMLs. Cellular immunotherapy is another treatment option for AML patients with specific cell surface markers including the Gentuzumab ozogamicin targeting CD33.