Special thanks to lead authors Danielle Bond and Sean Burnard and collaborators including @charles-debock.bsky.social, @mixomics.org and colleagues @hmriaustralia.bsky.social

These results show that AML therapies can increase epigenetic heterogeneity with implications for #cancer growth and treatment. By targeting the processes that help AML cells to re-initiate cancer growth, we may be able to delay AML progression.

Genes related to #cholesterol processes had increased expression in colonies formed after HMA exposure, regardless of the colony's methylation level. Targeting these processes with #statin co-treatment increased the efficacy of HMAs.

We show that some AML cells can evade the #epigenetic effects of these therapies and retain #DNAmethylation. We also found that HMA exposure alters transcription, even in highly-methylated cells.