[Subsequent AMKL evolves from a pre-existing TAM clone through the acquisition of additional mutations, with major mutational targets including multiple cohesin components (53%), CTCF (20%), and EZH2, KANSL1 and other epigenetic regulators (45%), as well as common signaling pathways, such as the JAK family kinases, MPL, SH2B3 (LNK) and multiple RAS pathway genes (47%).]. Sentence from MEDLINE/PubMed, a database of the U.S. National Library of Medicine.
Gene-disease associations inferred from text-mining the literature.
DisGeNET evidence - LITERATURE