D. C. J. Spierings

The paper tracks genome evolution in single-cell clones to reveal copy number alteration rates and features in cancer driven by chromosomal instability.

The paper investigates the effects of chronic SAC activation in mice, finding it causes bone marrow aplasia and intestinal atrophy, with BIM playing a critical role in gastrointestinal cell death.

The paper shows centrosome amplification in ovarian cancer cells primes them for apoptosis and improves chemotherapy response, independent of multipolar divisions and chromosome instability.

This study induces specific chromosome mis-segregation in human cells using CRISPR-Cas9 to create designer karyotypes and study aneuploidy's cellular effects.

The paper applies a clinically-relevant chemotherapy regimen to neuroblastoma PDX models to identify transcriptional patterns and mechanisms of chemoresistance.

The paper identifies Stat1 inactivation as a mechanism by which aneuploid cancers evade immune surveillance in mice and humans.

This study shows PARP inhibitors induce sister chromatid exchanges (SCEs) through under-replicated DNA processed in mitosis, independent of homologous recombination factors.

This study investigates how different aneuploidies affect chromosomal instability in human cells, finding that trisomies increase segregation errors while monosomies do not induce CIN.

This study shows that newly formed tetraploid human cells experience high DNA damage during the first S-phase, leading to abnormal karyotypes and genetic instability.

The paper investigates how replication stress alters histone deposition asymmetry on sister chromatids, showing a shift from lagging to leading strand bias.

This study shows that aneuploidy-induced genome instability helps cancer cells resist chemotherapy by enabling survival under drug pressure.

This study shows that PIDDosome-mediated ploidy restriction prevents hepatocellular carcinoma by reducing tumor burden and that low ploidy predicts poor survival in HCC patients.

This study investigates how TP53 promoter swapping in osteosarcoma leads to dysregulated gene expression and oncogenic activation.

The paper identifies synergistic toxicity between microtubule dynamics alteration and SAC inhibition in aneuploid cells.

The paper shows that human chromosome mis-segregation is non-random, with specific chromosomes showing higher rates of aneuploidy due to cohesion fatigue.

This study shows that BLM helicase suppresses recombination at G-quadruplex motifs in transcribed genes, preventing genomic instability in human and murine cells.