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Articles by Matthew Deyell
Global regulators facilitate adaptation to a phenotypic trade-off
Abstract Organisms depend on their ability to balance multiple phenotypes by evolutionary adaptation. For instance, cellular growth and movement jointly enable critical processes including microbial colonization and cancer invasiveness. Growth and movement are known to be controlled by local regulators that target single operons, as well as by global regulators that impact hundreds of genes. However, how these different levels of regulation interplay during evolution is unclear.
Adaptation to a phenotypic trade-off requires an interplay between local and global regulators
Abstract The fitness of organisms depends critically on regulatory strategies that balance multiple phenotypes, including physiological, developmental, and pathogenic. An important example is the trade-off between motility and growth determine competition for habitat colonization by microorganisms and the invasiveness of metastatic cells in cancer. Phenotype regulation relies on hierarchical gene networks, but how gene hierarchy contributes to adaptation remains unclear.
Non-cell-autonomous cancer progression from chromosomal instability - Nature
Abstract Chromosomal instability (CIN) is a driver of cancer metastasis1,2,3,4, yet the extent to which this effect depends on the immune system remains unknown.
Unjamming tumour cell invasion through cGAS–STING - Nature Materials
Locally confined epithelial malignancies undergo a phase transition from a solid-like to liquid-like state, a process called unjamming, where associated chronic intracellular strain causes nuclear envelope rupture, leading to the emergence of pro-metastatic traits due to cGAS–STING pathway activation. Malignancies that form from normal epithelium are frequently constrained into densely packed, or jammed, masses by the surrounding tissue.
Cancer metastasis as a non-healing wound
Abstract Most cancer deaths are caused by metastasis: recurrence of disease by disseminated tumour cells at sites distant from the primary tumour. Large numbers of disseminated tumour cells are released from the primary tumour, even during the early stages of tumour growth. However, only a minority survive as potential seeds for future metastatic outgrowths.
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