H4K20me3-Mediated Repression of Inflammatory Genes Is a Characteristic and Targetable Vulnerability of Persister Cancer Cells.

Anticancer therapies can induce cellular senescence or drug-tolerant persistence, two types of proliferative arrest that differ in their stability. While senescence is highly stable, persister cells efficiently resume proliferation upon therapy termination, resulting in tumor relapse. Here, we used an ATP-competitive mTOR inhibitor to induce and characterize persistence in human cancer cells of various origins.

The CellPhe toolkit for cell phenotyping using time-lapse imaging and pattern recognition.

With phenotypic heterogeneity in whole cell populations widely recognised, the demand for quantitative and temporal analysis approaches to characterise single cell morphology and dynamics has increased. We present CellPhe, a pattern recognition toolkit for the unbiased characterisation of cellular phenotypes within time-lapse videos. CellPhe imports tracking information from multiple segmentation and tracking algorithms to provide automated cell phenotyping from different imaging modalities, including fluorescence.

Corrupted devolution: How normal cells are reborn as cancer precursors.

Cancers are genetically divergent but intriguingly display similar patterns of epigenetic deregulation, including global DNA hypomethylation and hypermethylation of promoter CpG islands. Early developmental programmes mirror this cancer epigenome suggesting that reactivation of embryonic programmes is essential to the initiation of cancer. We propose a scenario where two waves of dedifferentiation underlie key cell transitions: the first from normal to cancer, and the second driving malignancy.