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Jay Moore

(He/Him)

Research Assistant

Mapping cell-type-specific vulnerability by integrating large-scale genomic and neuropathological data.

Biography

Over the past seven years, I have moved from cancer genomics to drug development to neurodegeneration, using data to make biological discoveries at scale. Across my work (10+ publications, 2 patents), I focus on applying computational approaches to identify structure in complex biological systems and translate it into insights in human health.


I developed HRD-Sig, a pan-cancer biomarker derived from pattern analysis of over 260,000 cancer genomes, now used routinely in clinical profiling at the largest clinical cancer genomics profiling company in the U.S, Foundation Medicine (Roche). I then moved to London to join a five person drug discovery startup, where I led transcriptomic analyses to investigate mechanisms of action and supported cell therapy programmes. I subsequently transitioned to academia through an MSc at the Great Ormond Street Institute of Child Health (UCL), focusing on biomarker development and gene therapy in rare disease.


I am now applying this approach in the Skene lab, working to advance the quantitative understanding of the cellular degeneration in Parkinson’s disease. In parallel, I am interested in large-scale genomic datasets and developing agentic-AI for biology research, including work with ClawBio.

Research interest

My research in the Skene lab has two arms. The first is a systematic review and meta-analysis of 189 neuropathology studies in Parkinson's disease, producing a new quantitative framing of selective vulnerability as a threshold effect on neuronal reserve rather than accelerated loss. 


The second is scaling MAGMA cell-typing into a systematic programme that maps which cell types underpin genetic risk across the full space of human GWAS, benchmarked against proteomic and rare-variant data and released as an open resource. 


Alongside this, I develop agentic-AI tooling for the lab and the broader ClawBio project, building the analytical infrastructure needed to keep pace with the frontier of neurodegeneration research.

Key publications

Cancer Discov
Published

Somatic HLA Class I Loss Is a Widespread Mechanism of Immune Evasion Which Refines the Use of Tumor Mutational Burden as a Biomarker of Checkpoint Inhibitor Response.

Authors
Meagan Montesion, Karthikeyan Murugesan, Dexter X Jin, Radwa Sharaf, Nora Sanchez, Ameet Guria, Max Minker, Gerald Li, Virginia Fisher, Ethan S Sokol, Dean C Pavlick, Jay A Moore, Alan Braly, Gaurav Singal, David Fabrizio, Leah A Comment, Naiyer A Rizvi, Brian M Alexander, Garrett M Frampton, Priti S Hegde, Lee A Albacker
Somatic HLA Class I Loss Is a Widespread Mechanism of Immune Evasion Which Refines the Use of Tumor Mutational Burden as a Biomarker of Checkpoint Inhibitor Response.