Still time to register!

Looking forward to a lively discussion!

Editors’ Picks, March 2026: Pediatric Leukemia Development, Low-dose Tamoxifen Use, and More In March, AACR's journals editors highlighted studies on the development of pediatric leukemia, the use of low-dose tamoxifen, and more.

Editors’ Pick by Cancer Research Catalyst @aacrjournals.bsky.social

RAS-driven plasticity and oncofetal reprogramming as a key mechanism and vulnerability in JMML.

The article is freely available for a limited time:
www.aacr.org/blog/2026/03...

#hematology
#oncology
#epigenetics
#development

Looking forward to a great scientific program with @bethpsaila.bsky.social, Simón Méndez-Ferrer, Jian Xu and many more exciting short talks.

Join us on April 16 to discuss developmental programs in leukemia.

@isehsociety.bsky.social

Excited to present our work at the 2026 #ISEH Mini Symposium!

“Beyond the Maturation Block: Oncofetal Reprogramming and Stem Cell Plasticity in Pediatric Leukemia”

Join us on April 16 to discuss developmental programs in leukemia and beyond.
iseh.org/Webinars-Eve...

JMML stem cells aren’t epigenetically “stuck” in a fetal state.

They mature postnatally—yet show striking transcriptional plasticity, with oncofetal reprogramming in high-risk disease, challenging the classic “maturation block” model.
doi.org/10.1158/2643...

#JMML #epigenetics #hematology #cancer

Same mutation ≠ same leukemia.

Wagenblast et al. show:
• fetal HSCs readily transform
• postnatal HSCs become resistant
• fetal programs create targetable vulnerabilities

Ontogeny matters: state-of-origin shapes biology & therapy response.
doi.org/10.1158/2159...

#pediatric #AML #stemcells

New Spotlight in @aacrjournals.bsky.social

#Oncogene × #Ontogeny × #Plasticity shape leukemia biology & therapy response.

Two complementary studies show: mutations alone don’t explain disease behavior—developmental state and cellular plasticity matter.

aacrjournals.org/bloodcancerd...

🩸🧬
EpiSci

You keep us on tenterhooks, what are those exciting discoveries??? 😲

Looking forward to find out more, hopefully some time soon.
😉

Absolutely, we see pronounced fetal signatures in JMML, too:

aacrjournals.org/bloodcancerd...

Unfortunately, LIN28B is not well captured in the scRNA data. However, I remember clusters revealing pronounced b-catenin expression patterns.
Will check this again… maybe we can find shared programs.

Exciting topic! Looking forward to reading this preprint.

Very pleased to share our latest pre-print which showcases the incredible hard work and skill of Dr Okan Sevim.

Our continued exploration of β-catenin's contribution to the post transcriptional landscape of blood cells led us to a LIN28B interaction.

1/7

www.biorxiv.org/content/10.6...

Congratulations, Julius and all Co-Authors!

🚨We have an opening for Data Scientists or Bioinformaticians using machine learning and AI with all kinds of molecular data to support cancer research. 🧬
Permanent position, fantastic team, exciting projects—what more could you ask for?
www.lih.lu/en/job/?valu...

Out in print this week @bloodjournal.bsky.social . Very proud of this collaborative work with Prof Karadimitris @imperialimmuno.bsky.social. Thanks to @cancerresearchuk.org and CwC_UK for funding this work. #InfantALL @paediatrics.ox.ac.uk @imm.ox.ac.uk

Thanks for sharing our study!

#Kinderkrebs
#Leukämie
@dkfz.bsky.social
@nct-heidelberg.bsky.social

Interesting story about the role of #oncofetal RNA-binding proteins in #immune #evasion in #ovarian #cancer.

Epigenetics that matters! Very cool work on hard to hard-to-access cell types . Finally some solid epigenetics examples that should be used in textbooks! Congrats to Mathieu and team @embl.org Rome!

Neue Erkenntnisse zu frühkindlicher Leukämie: Leukämiezellen können Programme aus der fetalen Entwicklung erneut aktivieren. Die Ergebnisse eröffnen neue Angriffspunkte für Diagnostik und Therapie.
www.nct-heidelberg.de/das-nct/news...

@dkfz.bsky.social @mphartmann.bsky.social @dblipka.bsky.social

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.