Epigenetics in acute myeloid leukemia

Acute myeloid leukemia (AML) is the most common type of leukemia in adults, characterized by uncontrolled proliferation of abnormal myeloid progenitor cells. Epigenetic alterations, such as DNA methylation or histone modifications, are likely to play a critical role in the initiation and progression of AML. Several studies have found that 70% of recurring mutations in patients with AML occur in gene expression regulators, such as epigenetic proteins, transcription factors, and splicing machinery components1-4. Furthermore, several epigenetics therapies, including DNA hypomethylating agents, have been approved by regulatory authorities worldwide or are now undergoing early-phase clinical trials5.

To help you study epigenetic mechanisms in AML, the poster covers all key established and promising epigenetics targets in acute myeloid leukemia, including:

• Histone modifications, such as H2AR3, H3K4, H3K36, H3K27, H3K9, H3R8, H3K79, H4R3
• Histone methylation/demethylation enzymes, including EZH2, KMT2A, SETD2, G9A (EHMT2), PRMT1, PRMT5, and DOT1L
• DNA methylation enzymes, such as DNMT3A, TET1/2/3, IDH1, IDH2
• Transcription factors, such as HOXA9, PU1, CEBPA, and RUNX1
• RNA binding proteins, including RBM39, IGF2BP1, Musashi 2, hnRNP K, NCL, WT1
• RNA methyltransferase METTL3
• Epigenetic reader BRD4

Once you’ve downloaded the poster, click on the highlighted epigenetic targets to access the range of corresponding products.