Thomas Oellerich

This study identifies phosphorylation as a mechanism protecting oncogenic RAS from LZTR1-mediated degradation, with implications for targeting RAS stability in hematologic cancers.

This study shows AML cells use extracellular protein catabolism to supply amino acids and manage nitrogen, with GS/GLUL playing a key role in ammonia buffering and disease progression.

This study maps tRNA expression dynamics across human hematopoiesis using sc-STM-seq and identifies tRNAs linked to stemness, differentiation, and cell lineages.

This study identifies CEBPA-N-AML as having enhanced engraftment and defines a novel LSC signature in CEBPA-N-AML.

PACMON integrates multi-omics data from perturbation screens to infer pathway-level responses to experimental perturbations, achieving high accuracy and scalability.

The paper identifies USP48 as a regulator of chromatin stability and DNA damage response to hypomethylating agents, showing its loss increases susceptibility to these drugs in AML.

The paper identifies a JAK2-HNRNPA1 pathway that represses retrotransposon activity in haematopoietic stem cells, reducing insertional mutagenesis.

This paper designs and tests sEH-PROTACs to degrade soluble epoxide hydrolase, identifying PROTAC 23 as effective in degrading sEH in human macrophages.

This paper engineers AAV9 vectors to selectively deliver genes to specific tumor cell subsets, demonstrating efficacy in preclinical cancer models and clinical relevance.

GeneCOCOA identifies context-specific functions of individual genes using co-expression data and curated functional gene sets, outperforming existing methods in gene-disease association recall.