Ian R. Powley

This study identifies YBX3 as an oncoprotein in mesothelioma that drives cell proliferation through SLC7A5/LAT1-mediated amino acid uptake and shows JPH203 as a potential therapeutic agent.

This study identifies mTORC2 as a convergent dependency in lung cancer that stabilizes HIF-1β to drive metabolic adaptation and tumor progression, revealing a therapeutic target in sphingolipid metabolism.

CYCLOPS provides an open-source platform for cyclic multiplex imaging and single-cell phenotyping using standard microscopy infrastructure, enabling reproducible and accessible spatial proteomics.

This study identifies architectural subtypes of PDAC using morphospatial profiling of CAFs, showing improved prognostication and chemotherapy response prediction.

This study uses spatial transcriptomics to analyze gene expression in lung adenocarcinoma morphologies, revealing plasticity and gene expression trajectories linked to lethal growth patterns.

This paper uses self-supervised AI to identify under-appreciated stromal morphologies in lung adenocarcinoma linked to poor prognosis, independent of current clinical schemas.

This paper introduces a self-supervised learning framework to analyze multiplex immunofluorescence images, revealing novel prognostic spatial patterns in cancer tissues.

This paper uses self-supervised learning on 3446 H&E-stained mesothelioma slides to create a histomorphological atlas, achieving high predictive performance and revealing molecular insights.

This study shows that increased mRNA translation delays lung adenocarcinoma initiation and creates a vulnerability to MEK inhibitors in KRAS-driven tumors.

This study identifies TNF- and TGF-β signaling as drivers of tumour budding in CRC, linked to poor prognosis and an immunosuppressive microenvironment.

PixlMap is a deep learning method for cellular phenotyping in multiplex immunofluorescence images that uses nuclear segmentation alone to classify cells without requiring full cell boundaries.

This study shows eIF4A1 is critical for supporting translational demands in Wnt-driven colorectal cancers, while eIF4A2 loss accelerates tumourigenesis, and eFT226 inhibits eIF4A1 function in these models.