Morag Park

This study identifies LOX as a driver of ccRCC progression by sustaining HIF-2α transcription and modulating the tumor microenvironment.

This study identifies 59 gene expression programs in RCC that reveal subtype identity and metastatic trajectories, including a metastatic signature linked to poor clinical outcomes.

The paper identifies an AMPK-FLCN-TFE3 pathway that promotes hypoxia survival through lysosomal and mitochondrial biogenesis, with implications for cancer therapy.

This study identifies ATR and PKMYT1 as targets to overcome carboplatin resistance in TNBC by re-sensitizing resistant models to carboplatin through mitotic catastrophe.

The paper identifies phosphorylation of membrane trafficking regulators, particularly SEC16A, as key to FER-mediated invasion in TNBC organoids.

The paper investigates the roles of TRIM28, DNA methylation, and p53 in regulating gene and transposon expression in human embryonic and trophoblast stem cells, revealing divergent responses to genomic instability.

This study maps the metabolic complex genetic interaction network of chromosome 4p loss in basal breast cancer to identify targetable vulnerabilities.

This study shows that EZH2 inhibition in TNBC causes metabolic stress, making cells more sensitive to glutaminase inhibitors.

This study shows AMPK regulates clathrin-mediated endocytosis by controlling Dab2 and Arf6 to selectively internalize β1-integrin.

The paper establishes a large-scale biobank of GEA patient-derived organoids that accurately model tumor features and drug responses, enabling personalized treatment strategies.

This study identifies a reversible basal-like cell state in AKT-inhibitor resistant triple negative breast cancer using multimodal profiling and lineage tracing.

The paper investigates the evolution of chromosome 4p loss in basal breast cancer, identifying C4orf19 as a novel gene that suppresses proliferation and is part of a kinase module.

This study identifies metabolic adaptations in taxane-resistant triple-negative breast cancer cells that lead to epigenetic vulnerabilities, specifically through altered methionine metabolism and H3K27me3 redistribution.

CrosstalkNet is a web-based tool for visualizing and analyzing large-scale bipartite co-expression networks to study tumor-stromal cell interactions.