Author

Leonie Smeenk

Erasmus MCORCID 0000-0001-7025-8515Unclaimed ORCID profile · follow to get notified of new preprints

Biology Disciplines

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Signature Assays, Organisms & Methods

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Organism:human· 3 Assay:bulk RNA-seq· 2 Research Focus:cell type annotation· 2 Approach:deep learning· 2 Research Focus:differential expression· 2 Research Focus:drug response / drug discovery· 2 Research Focus:gene regulatory network inference· 2 Approach:statistical model· 2

Frequent Co-Authors

Roger Mulet‐LazaroiD· 3 shared Ruud DelweliD· 3 shared Claudia A. J. Erpelinck-VerschuereniD· 2 shared Dorien PastoorsiD· 2 shared Eric M. BindelsiD· 2 shared Marije HavermansiD· 2 shared Torsten HaferlachiD· 2 shared Anastasija PejkovskaiD· 1 shared

Activity by Year

2024-2025 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 36 mutual co-author links

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3 shared papersCancer Biology

Roger Mulet‐LazaroORCID

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3 papers

Recent·Most cited

Cancer BiologyBloodPeer-reviewedOct 8, 2025

MECOM is a master repressor of myeloid differentiation through dose control of CEBPA in acute myeloid leukemia

Dorien Pastoors, Marije Havermans, Roger Mulet‐Lazaro…·Ruud Delwel

This study shows MECOM represses myeloid differentiation by inhibiting CEBPA, and its overexpression in AML reduces CEBPA levels, maintaining stem cell state.

8 citationstop 3%

humanbulk RNA-seq

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Cancer BiologyBlood Cancer DiscoveryPeer-reviewedMar 31, 2025

Pyjacker identifies enhancer hijacking events in acute myeloid leukemia including MNX1 activation via deletion 7q

Etienne Sollier, Anna Riedel, Umut H. Toprak…·Christoph Plass

Pyjacker detects enhancer hijacking in AML, identifying MNX1 activation via 7q deletion as a novel oncogenic mechanism.

8 citationstop 4%

humanbulk RNA-seq

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Cancer BiologyScience AdvancesPeer-reviewedMay 15, 2024

Oncogene EVI1 Drives Acute Myeloid Leukemia Via a Targetable Interaction with CTBP2

Dorien Pastoors, Marije Havermans, Roger Mulet‐Lazaro…·Ruud Delwel

This study identifies EVI1's interaction with CTBP1/CTBP2 as critical for AML and shows that inhibiting this interaction can block leukemic growth.

17 citationstop 4%

humanproteomics

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