Thank you so much for featuring our work!! Really enjoy your podcast, @stemcellpodcast.com!

Congratulations, @kmachlus.bsky.social and team!!!

🙏 🙏 Thank you so much, @cherisirois.bsky.social!!!

So perhaps in the future by better understanding these pathways, we could develop targeted differentiation strategies for inv(3) leukemia. Reading Tatiana's essay in @newyorker.com is incredibly inspiring. (fin)

Recently, @tjflemin.bsky.social from our lab, along with @dpastoors.bsky.social + @delwelruud.bsky.social, showed that MECOM represses pro-differentiation factors in AML, particularly CEBPA. Reexpressing CEBPA can force differentiation of these AMLs: tinyurl.com/4tckppkh, tinyurl.com/yck4hbk9 (6/n)

But how does MECOM do this and might there be opportunities to therapeutically intervene by understanding this? (5/n)

By following up on clues from a rare genetic disease, Richard Voit from our group showed that MECOM was critical for enabling 🩸stem cell gene programs to be expressed and these were co-opted in high-risk leukemias: nature.com/articles/s41... (4/n)

In 2014, two groups, including one led by @delwelruud.bsky.social, showed that inv(3) juxtaposes an enhancer of GATA2 to drive high expression of MECOM/EVI1: cell.com/cell/fulltex..., cell.com/cancer-cell/... (3/n)

Several studies have shown how inv(3) leukemia, which is associated with high expression of MECOM (a.k.a. EVI1), has a poor prognosis: ascopubs.org/doi/10.1200/... (2/n)

Congratulations, @pgtimmune.bsky.social!!!

Congratulations, @igorulitsky.bsky.social!!!

Congratulations, @trevorgraham.bsky.social and team!!!