Thomas Milne

Thomas Milne has made critical contributions to understanding how MLL (mixed-lineage leukemia) gene rearrangements drive acute leukemia through aberrant histone H3K4 methylation and recruitment of transcriptional elongation machinery. His laboratory elucidated how MLL fusion proteins hijack the normal H3K4 methyltransferase function to activate HOX gene programs that block hematopoietic differentiation and promote leukemic self-renewal. He has contributed to the development of therapeutic strategies targeting MLL-rearranged leukemia, including menin-MLL interaction inhibitors and DOT1L H3K79 methyltransferase inhibitors. His work connects histone modification enzymology to clinical leukemia biology.