Peter Ly

TL;DR: It is shown that chromosomally unstable tumour cells co-opt chronic activation of innate immune pathways to spread to distant organs by sustaining a tumour cell-autonomous response to cytosolic DNA.

TL;DR: DNA sequence-dependent binding of CENP-B within α-satellite repeats is required to stabilize optimal centromeric levels of C ENP-C, and data demonstrate a DNA sequence-specific enhancement by CENp-B of the fidelity of epigenetically defined human centromere function.

TL;DR: An inducible Y centromere-selective inactivation strategy is developed by exploiting a CENP-A/histone H3 chimaera to directly examine the fate of missegregated chromosomes in otherwise diploid human cells, and initial errors in cell division can provoke further genomic instability through fragmentation of micronuclear DNAs coupled to NHEJ-mediated reassembly in the subsequent interphase.

TL;DR: In this paper, the authors used whole-genome sequencing of clonal cell isolates that developed chemotherapeutic resistance to show that chromothripsis is a major driver of circular extrachromosomal DNA (ecDNA) amplification through mechanisms that depend on poly(ADP-ribose) polymerases (PARP) and the catalytic subunit of DNA-dependent protein kinase (DNA-PKcs).

TL;DR: Emerging mechanisms underlying chromothripsis are reviewed with a focus on the contribution of cell division errors caused by centromere dysfunction, and the role of DNA double-strand break repair during the subsequent interphase.