Kimberly Stegmaier

The paper presents an unbiased surfaceome atlas of leukemic cell lines, identifying novel surface proteins and discordant gene expression patterns, with CD70 highlighted as a potential therapeutic target in AML.

The paper identifies a core regulatory circuit in rhabdomyosarcoma and shows that targeting two co-activators synergistically inhibits tumor growth.

This study identifies CDK8 inhibition as a therapeutic strategy for alveolar rhabdomyosarcoma by inducing myogenic differentiation and impairing tumor growth through a mechanism involving the Mediator kinase module, SAGA complex, and SIX4.

The paper develops ALTitude, a machine learning model to predict ALT status from whole genome sequencing data, identifies SMARCAL1 as a therapeutic target in ALT-driven cancers.

This paper identifies a bifunctional small molecule that can induce both transactivation and repression of gene expression depending on cellular context.

This study identifies MECOM's role in blocking differentiation via CEBPA repression, showing that targeting this regulatory element can promote differentiation and reduce leukemia burden in AMLs.

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.

This study shows that inhibiting KAT6A/B with PF-9363 enhances retinoid efficacy and improves GD2-targeted immunotherapy in neuroblastoma.

This study identifies riboflavin as a critical metabolic dependency in acute myeloid leukemia, showing its role in nucleotide biosynthesis and iron-sulfur cluster metabolism beyond energy production.

This study identifies IRF2BP2 cytoplasmic sequestration by MCL1 as a mechanism driving venetoclax and azacitidine resistance in AML through ACSL1 derepression.

This study develops a bivalent small molecule, EB-TCIP, that relocalizes EWS/FLI1 to induce BCL6 target genes, demonstrating a strategy to target fusion oncoproteins in Ewing sarcoma.

The paper identifies ARGOS genes, which are amplified in cancer, have low expression relative to copy number, and are toxic when overexpressed, and validates several as pan-cancer targets.

This paper identifies cell state-dependent and -independent immunotherapeutic targets in neuroblastoma by analyzing subtype-specific gene expression and validating targets through experimental methods.

The paper benchmarks six MYB inhibitors using a nascent transcriptomics assay, revealing partial specificity, off-target activity, and mixed agonism-antagonism effects.

The paper reconstructs a sparsely interconnected transcriptional hierarchy in leukemia cells stabilized by incoherent feed-forward loops and shows inhibitors disrupt core regulators' programs.

The paper identifies transcription factors regulating MHC-II expression in AML and shows their role in immune evasion and relapse.

The paper identifies a modular core regulatory circuitry in AML that enforces oncogene expression in KMT2A-rearranged leukemias.

The paper develops CERES, a computational method to correct copy-number effects in CRISPR-Cas9 essentiality screens, improving specificity in cancer cell line studies.