Mark Hartmann

Mark Hartmann

@mphartmann.bsky.social

Scientist at DKFZ and NCT Heidelberg #epigenetics #stemcells #leukemia #colorectalcancer #multiomics #precisiononcology #oncofetal #reprogramming #plasticity www.translational-cancer-epigenomics.de

1.8K followers4.4K following106 posts

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Genetics and methylomes largely agreed, but not completely: two CTC subpopulations emerged, with two cells assigned differently across layers. Transcriptomes supported neuroendocrine identity without clearly separating these groups.

Each molecular layer adds a different perspective. This single-patient proof of concept shows how simultaneous multi-omics connects CTC identity with heterogeneity—and reveals where genetic, epigenetic and transcriptional patterns agree or diverge.

Which rare circulating cells are tumour cells? In a patient with metastatic cervical small-cell neuroendocrine carcinoma, tumour-matched genetic alterations and complementary methylation and RNA profiles established CTC identity.

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

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

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...

iseh.org Mini Symposium

We are excited to announce the full Mini Symposium program featuring the short talks selected from submitted abstracts! Don't miss the chance to view groundbreaking research and choose the top short talk. View the full program and register ➡️ iseh.org/Webinars-Eve...

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

doi.orgOntogeny Dictates Oncogenic Potential, Lineage Hierarchy, and Therapy Response in Pediatric LeukemiaAbstractAccumulating evidence links pediatric cancers to prenatal transformation events, yet the influence of the developmental stage on oncogenesis remains elusive. We investigated how hematopoietic ...

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

doi.orgMolecular Plasticity Results in Oncofetal Reprogramming and Therapeutic Vulnerabilities in Juvenile Myelomonocytic LeukemiaAbstractPersistent fetal gene expression in childhood neoplasms is usually explained by a maturation block originating in the prenatal phase. In contrast, reactivation of fetal genes in adult malignan...

Mark Hartmann reposted

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...

biorxiv.orgDual targeting a LIN28B:β-catenin axis in acute myeloid leukaemiaWnt/β-catenin signalling is dysregulated across several haematological malignancies, including acute myeloid leukaemia (AML), where is lacks effective targeting strategies. Previously, we discovered that β-catenin interacts with several RNA-binding proteins (RBP), and binds mRNA indirectly, indicating contributions to the post-transcriptional landscape of leukaemia cells. Here, we found the most frequent RBP-binding motif amongst β-catenin-bound mRNAs was the GGAG motif targeted by the oncofoetal expressed miRNA-regulating RBP LIN28B. We detected the β-catenin:LIN28B interaction in lymphoid and myeloid cell lines, and primary human CD34⁺ fetal liver-derived haematopoietic stem cells. LIN28B positively regulated Wnt signalling capacity by regulating LEF1 expression through a post-transcriptional mechanism requiring the let7 miRNA axis. Further miRNA sequencing of β-catenin- and LIN28B-depleted myeloid cells revealed both potential cooperative and antagonistic function in miRNA regulation. Finally, dual-targeting both β-catenin and LIN28B through either genetic or pharmacological means preferentially killed AML cells. These data reveal a potential novel synthetically lethal relationship in AML which could be exploited in the rare AML subsets where LIN28B expression becomes reactivated ### Competing Interest Statement The authors have declared no competing interest. Kay Kendall Leukaemia Fund, https://ror.org/03j2wfg84, KKL1051, KKL1446 Leukaemia & Myeloma Research UK, 4-5/06.21R Children’s Cancer & Leukaemia Group, CCLGA 2023 16 Morgan Republic of Türkiye Ministry of National Education

Mark Hartmann reposted

🚨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...

lih.luJob » Luxembourg Institute of HealthApplications including a letter detailing your motivation and a curriculum vitae should be sent through our website via the apply button below.

Mark Hartmann reposted

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

Blood Journals Portfolio@bloodjournals.hematology.org

Off-the-shelf bispecific CD133-CD19 CAR-iNKT cells eradicate CAR antigen–high and –low medullary and leptomeningeal KMT2Ar ALL. Read in Blood: buff.ly/HIlsUq7 #ALL #BloodJournal

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

Scientists identify #IGF2BP1 as a driver of #ImmuneEvasion in C5 #OvarianCancer, suppressing IFN‑γ–IRF1–MHC‑I signaling and T‑cell infiltration; its inhibition restores #antitumor immunity and boosts #PD1blockade. @unihalle.bsky.social #OpenAccess in #STTT: doi.org/10.1038/s413...

Mark Hartmann reposted

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!

Jamie Hackett@jamiehackett.bsky.social

This went under the radar but answers a fundamental question in Epigenetics... From many hundreds of olfactory receptor genes, each neuron selects expression of only single one (near-randomly). How? Outstanding work from Mathieu Boulard and colleagues www.biorxiv.org/content/10.6...

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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.

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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.

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

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.

Pioneers of Epigenetics honored: Davor Solter & Azim Surani receive the 2026 Paul Ehrlich & Ludwig Darmstaedter Prize. Their discovery of genomic imprinting revealed why mammals need both parents—opening the field of epigenetics. #Epigenetics #GenomicImprinting #PaulEhrlichPrize #CanSky #Science

The German Science and Humanities Council declares permanent positions the new standard. Interview with @wickwolfgang.bsky.social & Insa Großkraumbach @wissenschaftsrat.de A must-read for all working in higher education and research in Germany! #Wissenschaft #Forschung #WissZeitVG #IchBinHanna

Jan-Martin Wiarda@jmwiarda.bsky.social

Schluss mit "Up or Out" Der Wissenschaftsrat erklärt Dauerstellen zum Regelfall. Ein Paukenschlag vor der Novelle des Wissenschaftszeitvertragsgesetzes. Im Interview erklären Wolfgang Wick und Insa Großkraumbach, was das bedeutet. Im Wiarda-Blog: www.jmwiarda.de/blog/2025/07...

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Entscheidend wird sein, dass Projektbezüge nicht weiter als formale Begründung für Befristungen dienen – ein strukturelles Problem, das das #WissZeitVG bislang erlaubt. Jetzt ist die Chance, das zu ändern. #Hochschulpolitik #Forschung

„𝗪𝗶𝗿 𝗯𝗿𝗮𝘂𝗰𝗵𝗲𝗻 𝗲𝗶𝗻𝗲 𝗴𝗿𝘂𝗻𝗱𝗹𝗲𝗴𝗲𝗻𝗱𝗲 𝗥𝗲𝗳𝗼𝗿𝗺.“ „𝗗𝗮𝘀 𝗦𝘆𝘀𝘁𝗲𝗺 𝗶𝘀𝘁 𝗻𝗶𝗰𝗵𝘁 𝗻𝘂𝗿 𝗶𝗻𝘁𝗿𝗮𝗻𝘀𝗽𝗮𝗿𝗲𝗻𝘁, 𝘀𝗼𝗻𝗱𝗲𝗿𝗻 𝗮𝘂𝗰𝗵 𝘇𝘂𝗻𝗲𝗵𝗺𝗲𝗻𝗱 𝘂𝗻𝗮𝘁𝘁𝗿𝗮𝗸𝘁𝗶𝘃.“ @wickwolfgang.bsky.social, Vorsitzender des Wissenschaftsrats #Wissenschaft #Forschung

In der PM heißt es: Daueraufgaben sollen zu unbefristeten Stellen führen – genannt werden v. a. IT, Infrastruktur, Wissenschaftsmanagement. Das ist gut, aber: Die wissenschaftliche Fachexpertise darf nicht fehlen. #WissZeitVG

Fascinating!

Sergio Cruz-León@sergiocruzleon.bsky.social

Excited to share our preprint on the molecular architecture of heterochromatin in human cells 🧬🔬w/ @jpkreysing.bsky.social, @johannesbetz.bsky.social, @marinalusic.bsky.social, Turoňová lab, @hummerlab.bsky.social @becklab.bsky.social @mpibp.bsky.social 🔗 Preprint here tinyurl.com/3a74uanv