Stem cell-like states confer poor outcomes in blood cancer—but what mechanisms drive this and how can they be therapeutically targeted? In our new preprint, we show how a single TF represses one enhancer to maintain a subset of high-risk leukemias: 🧵👇.

Joining the Voit Lab is the best decision you will ever make. Go work with Richard if you can!.

RT @RichardVoit: We at are grateful to @TexasCCF for supporting our work. Thank you also to @dallascowboys @dak, @….

super fun game from the inimitable @ernstschmidd - check it out!.

RT @UCSDmbb: A season to remember, and it's just our beginning. 🔱. #GoTritons

RT @MolecularCell: Predictomes, a classifier-curated database of AlphaFold-modeled protein-protein interactions htt….

RT @ISEHSociety: Alessandro Donada sat down with @d_pastoors and @tjflemin for a deep dive on their latest AML biology preprints. Watch the….

RT @ernstschmidd: In our tests, SPOC outperforms other commonly used metrics in prioritizing biologically relevant interactions in large sc….

RT @ernstschmidd: Very excited to share that my thesis work is out in Molecular Cell! We trained a Structure and Omics informed Classifier….

RT @LWahlster: I am grateful to @DamonRunyon @StJude for supporting my work and to @bloodgenes for the mentorship🙏 Very excited to meet my….

RT @GongDennis: Excited to share my analysis of the Cancer Dependency Map!. My goal was to systematically identify biomarker - dependency r….

RT @LWahlster: I am grateful to be a part of this amazing group. Thank you to @ASH_hematology for supporting my research and career develop….

A complementary pre-print was also posted from @DelwelRuud and @d_pastoors further highlighting the importance of MECOM's repression of CEBPA in AML!

RT @DelwelRuud: Excited to share our preprint (@D_Pastoors): "MECOM is a master repressor of myeloid differentiation through dose control o….

RT @bloodgenes: Wonderful to have this work led by @tjflemin along with other colleagues in our laboratory, as well as great collaborators,….

Joao Paulo, @GygiLab, @camimoso, @AdelmanLab, Jennifer Perry, @PikmanYana, @KStegmaier_DFCI, @nubama, @theclotthickens, @hovestadt, Andrea Arruda, Mark Minden, and @RichardVoit.

Just as important, none of this work could have been possible without immense help and mentorship from my good friends, collaborators and co-authors: @mateusz_ant, Sander Lambo, @therealDrGundry, Riccardo Piussi, @LWahlster, Sanjana Shah, Fiona Reed, @kevinduydong. .

This study is the culmination of my PhD thesis work in @bloodgenes’ lab. I am incredibly grateful for the amazing support and mentorship Vijay has provided me over the years, allowing me to freely pursue my scientific interests.

I’m incredibly optimistic that these approaches can be extended across other leukemias and solid tumors, enabling therapeutic differentiation of malignant cells by rewiring dysregulated transcriptional activity.

In summary, we demonstrate how synergistic use of targeted protein degradation, functional genomic perturbations, and high-throughput screens can distill the functional significance of a complex oncogenic signaling network into a single, pivotal gene regulatory node.

Strikingly, activating this cisRE significantly impaired the engraftment ability of primary AML cells, highlighting the therapeutic potential of reactivating myeloid differentiation programs to disrupt the fitness of stem cell-like leukemia cells.