Floris Foijer

This study shows that chromosomal instability (CIN) drives rapid genome changes in cancer cells, generating new copy number alterations each cell cycle and increasing genomic complexity.

This study shows that chromosome 7 gain optimizes WNT signaling in colorectal cancer by counteracting excessive stemness from APC mutations.

The paper shows that chromosomal instability (CIN) leads to distinct p21-expressing cell populations with different cell-cycle recovery and extracellular vesicle (EV) properties, resulting in increased migration.

This study shows that TET loss of function promotes aneuploidy, particularly chromosome 17 trisomy, which provides a proliferative advantage in iNKT cells and mESCs.

The paper identifies the SKA complex as a mitotic vulnerability in chromosomally unstable cancers, showing its selective impact on these cells through prolonged mitosis.

This study identifies Profilin 1 as a safeguard against genome doubling and polyploidy in cancer by showing its role in maintaining cell cycle fidelity and preventing therapeutic resistance.

This study shows that chromosomal instability in TNBC increases EV secretion and promotes cell migration via EFEMP1, identifying EFEMP1 as a potential therapeutic target.

This study shows that chromosomal instability in esophageal adenocarcinoma drives an inflammatory tumor microenvironment through a cGAS-chemokine-myeloid axis, with CXCL8 as a key mediator.

This study shows that BLM helicase is essential for resolving ultrafine DNA bridges during mitosis, preventing genomic instability.

This study shows that low-dose GSK3 inhibitors prevent aneuploidy in hPSCs by reducing mitotic DNA synthesis and ultra-fine chromosome bridges during long-term culture.

This study benchmarks six scRNA-seq CNV callers using 15 datasets, finding that reference choice and allelic information impact performance, with some methods being more robust but computationally intensive.

The paper shows that increased PRMT5-MEP50 complex activity helps aneuploid cancer cells survive by reducing protein aggregation and proteotoxicity.

This study characterizes tertiary lymphoid structures in endometrial cancer using multi-level transcriptomics, identifying transcriptional signatures and immune cell dynamics linked to ICI response.

The paper shows that CDK4/6 inhibitor-treated cells that evade senescence experience mitotic errors and aneuploidy due to cell enlargement, which can be rescued by restoring cohesion.

This study shows that BTRR complex deficiency increases genomic instability through copy number alterations, enriched at fragile sites, using CRISPR-edited iPSC models.

The paper identifies ARGOS genes, which are amplified in cancer, have low expression relative to copy number, and are toxic when overexpressed, and validates several as pan-cancer targets.

The paper identifies CDC20 expression as a determinant of sensitivity to SAC inhibitors, showing that aneuploid cells with high CDC20 levels are more sensitive to these drugs.

This study identifies four subgroups of osteosarcomas based on genomic and transcriptomic analysis, revealing distinct mechanisms of CDK4 amplification in relation to MDM2 or TP53 alterations.

The paper shows centrosome amplification in ovarian cancer cells primes them for apoptosis and improves chemotherapy response, independent of multipolar divisions and chromosome 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 tracks genome evolution in single-cell clones to reveal copy number alteration rates and features in cancer driven by chromosomal instability.

This study shows that IFNγ treatment reduces apoptosis and improves translation rates in ALS6 patient-derived motor neurons under oxidative stress.

This study uses tunable DNMT1 degradation to investigate DNA methylation dynamics and genome organization, revealing cooperative roles of DNMT1 and DNMT3B and their impact on heterochromatin and cell fitness.

The paper identifies HDAC4 as a synthetic lethal target in MELK-overexpressing cancers through a yeast screen and mammalian validation.

This study shows that SERF2 deletion changes amyloid fibril structure in Alzheimer's mouse models, suggesting SERF's role in modifying amyloid aggregation.

The paper identifies DNA copy number alterations and chromosome-scale losses caused by replication stress in non-transformed cells, revealing their role in chromosomal instability and cancer evolution.

The paper shows that gene regulatory networks inferred from cancer data are heavily influenced by aneuploidies and sample impurities, with up to 80% of edges potentially due to these factors.

This study uses single-cell DNA sequencing to identify distinct molecular types of basal cell carcinoma based on karyotype heterogeneity and associated transcriptome features.