James M. Ford

This study shows that many premalignant colorectal polyps contain multiple genetic lineages, indicating polyclonal origins rather than single-cell expansion.

This study identifies a four amino acid motif in VISTA that suppresses tumor growth by altering EGFR signaling through NUMB recruitment.

The paper uses spatial CODEX experiments to show early colorectal cancer microenvironment changes in FAP, including CAFs, immune suppression, and beta-catenin nuclear translocation.

This study shows that early colorectal cancer loses promoter-enhancer connectivity, leading to gene expression changes and a two-phase model of transcriptional regulation.

The paper describes the development of a gastric cancer registry integrating clinical and genomic data to support translational research.

The paper uses ultra high-throughput methylation sequencing to study DNA methylation changes during colorectal cancer progression from normal tissue to adenocarcinoma.

The paper uses single-cell data to show a continuum of cell state and composition changes from polyps to colorectal cancer, identifying stem-like cells and regulatory markers.

The paper identifies TP53 genomic deletions as a poor prognosis marker in Stage III colorectal cancer using a new low-coverage whole-genome sequencing protocol.

This paper identifies HAT1 as a gene that links nutrient metabolism to histone production through a gene-metabolite circuit, showing its role in cell proliferation and its association with cancer outcomes.

The paper uses long-read whole genome sequencing to identify a pathogenic structural variant in a patient with Carney complex, demonstrating the potential of LRS in diagnosing Mendelian diseases.