Uri Ben‐David

This study maps chromothripsis in 1,646 human cancer cell lines, showing its conservation with tumors, higher prevalence, and therapeutic vulnerabilities to HDAC inhibitors.

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 analyzes single-cell RNA sequencing data from 304 tumors to explore how aneuploidy affects cancer progression and cellular fitness.

The paper identifies NDE1 as a synthetic lethal target in metastatic cancer cells driven by chromosomal instability and Chr17p loss.

The paper shows that cell and nuclear size in tetraploid cancer cells correlate with chromosomal instability and tumorigenicity, with smaller cells having better fitness and poorer patient survival in WGD-positive cancers.

The paper shows that ribosome quality control via ZNF598 degradation helps aneuploid cells survive proteotoxic stress, with ZNF598 expression linked to tumor aneuploidy.

This study shows that p53 inactivation promotes breast cancer brain metastasis by altering fatty acid metabolism, with implications for therapeutic targeting.

This study identifies Del17p as a biomarker for AURKB inhibition in breast cancer, showing increased sensitivity to AURKB inhibitors in Del17p tumors.

The paper identifies 311 candidate driver genes for recurrent chromosome-arm losses in 20 cancer types using integrated gene expression, mutation, and copy number data from ~7,500 tumors.

This study shows p53 inactivation is not universally linked to aneuploidy but is associated with increased chromosome loss in cancer.

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.

The paper investigates the co-occurrence of chromosome 10 loss and chromosome 7 gain in gliomas, finding functional rescue interactions on chromosome 7 that may compensate for chromosome 10 loss.

The paper analyzes genetic changes in human pluripotent stem cells under different culture conditions and identifies a link between feeder-free culture and increased chromosome 1q gains.

This study shows that overexpressing human APOBEC3B in mice causes lethality through RNA editing and organ dysfunction.