Nicholas McGranahan

Odon is a fast, interactive viewer for spatial proteomics data that outperforms existing tools in loading and rendering large-scale imaging datasets.

This paper uses agent-based simulations to test models of lung tumour growth, finding that stringent cell competition after tumour size stabilization produces realistic clonal expansions and better estimates of driver mutation effects.

This study shows that LIMD1 loss in lung cancer increases PD-L1 expression, promoting immune evasion and enhancing response to immune checkpoint inhibitors.

The paper introduces MACH2, a method to systematically enumerate all plausible migration histories of metastatic cancers, outperforming existing methods and detecting extensive uncertainty in real cancer data.

This paper develops a signature, iHet, to capture tumor microenvironment heterogeneity linked to immune activity and evasion using transcriptomic data from lung cancer.

Refphase uses multi-sample reference phasing to infer haplotype-specific copy numbers and reveal intra-tumour heterogeneity in cancer samples.

cloneMap visualizes clonal heterogeneity in genomic data by representing clone size and phylogenetic relationships, applied to cancer datasets.

The paper investigates how anti-cancer immunity evolves from preneoplasia to invasive lung adenocarcinomas, identifying changes in immune response and molecular features that may facilitate immune evasion.

This study examines DNA methylation changes and intra-tumor heterogeneity in lung adenocarcinoma progression, finding increased methylation aberrations and immunosuppression in later-stage lesions.

This paper introduces CAMDAC, a method to deconvolve tumor-normal DNA methylation profiles while accounting for copy number changes, revealing epigenetic instability and distinct patterns in lung cancer.

The paper investigates how whole genome doubling (WGD) in cancer may mitigate Muller’s Ratchet by reducing negative selection on mutations in essential genes after duplication.

The paper investigates genetic epistasis in EGFR-mutant lung cancers using over 2,000 cases, showing that genetic combinations, not single drivers, dominate tumor progression and clinical outcomes.