Congratulations, Julius and all Co-Authors!

Thank you so much, Tim!!!

And I agree! Our first experience with Blood Cancer Discovery @aacrjournals.bsky.social was really really great. Very quick, communicative and professional, but also absolutely supportive, proactive, flexible and courteous!

Of course, it’s always a pleasure to talk to you! :)

Thanks, Tim!

I will let him know… ;) unfortunately, he’s not on bluesky.

@simonhaas.bsky.social
@mhaniffa.bsky.social
Jan-Philipp Mallm
Sam Behjati
Marc-Jan Bonder
@stefanfrohling.bsky.social
Elliot Stieglitz
Charlotte M. Niemeyer

Fatemeh Alikarami
@littleoldmewi.bsky.social
Jun Wang
Tobias Boch
@viktoriaflore.bsky.social
@pavlolutsik.bsky.social
@milsommick.bsky.social
Simon Raffel
Christian Buske

Jovana Rajak
Valentin Maurer
Ling Hai
Katharina Bauer
Mariam Hakobyan
Sina Stäble
Jens Langstein
Laura Jardine
Roland Roelz
Sheila Bohler
Eleonora Khabirova
Abdul-Habib Maag
Dominik Vonficht
Dirk Lebrecht
Katrin M. Bernt
@kaitanlab.bsky.social
Changya Chen

Fantastic environment at our host institutes @dkfz.bsky.social & @nct-heidelberg.bsky.social

Thanks to all co-authors of this publication:

Deep gratitude to

my friend and shared first co-author Maximilian Schönung

the last authors @joschkah.bsky.social, Christian Flotho, Christoph Plass, Miriam Erlacher, Matthias Schlesner, and especially @dblipka.bsky.social

Multi-omics integration reveals risk-associated gene expression signatures, identifying CD52 as a potential therapeutic target for high-risk JMML.

Anti-CD52 treatment depletes JMML stem cells and disrupts disease propagation in a JMML PDX model.

RAS-pathway mutations induce fetal-like gene expression programs in a JMML mouse model, suggesting RAS-driven oncofetal reprogramming in murine JMML stem cells.

Fetal HSC signatures are enriched in patients without detectable JMML driver mutations at birth.

JMML stem cells show transcriptional plasticity, hijacking parts of distinct developmental programs, including fetal HSC marker genes, leading to mosaic-like developmental expression programs.

This suggests the reactivation rather than preservation of oncofetal signatures.

The postnatal maturation state of JMML stem cells challenges the universality of the maturation block model in pediatric malignancies.

JMML epitypes are prognostic biomarkers in JMML.

Conservation of such disease-specific epigenetic signatures in HSC-like JMML stem cells and downstream immune cells suggests HSCs or early HSPCs as the cells-of-origin in JMML across JMML epitypes.

Epigenomes encode cell type, developmental state, and disease-specific information.

DNA methylomes of JMML stem cells reveal:

1. HSC-like cell type signatures
2. A postnatal maturation state
3. Disease-specific epitypes

Congratulations, Rolf & Team!
Very interesting story!