R. H. Medema

This study shows that aneuploid cancer cells adapt by reducing chromosomal instability and inflammation, with KRAS amplification aiding this adaptation.

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.

This study shows that inhibiting PP2A and WEE1 together can kill colon cancer cells by causing DNA replication collapse and cell death, and that resistance to this treatment suppresses tumor growth.

This study shows MND1 facilitates repair of two-ended DNA double-strand breaks in somatic cells through homologous recombination, but not one-ended breaks, and its absence increases IR-induced toxicity.

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

The paper identifies that combining indisulam with palbociclib enhances senescence in cancer cells by inhibiting CDK2 kinase activity.

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

The authors withdrew their manuscript due to inconsistencies in data and questionable experimental results regarding DNA end-resection and chromatin accessibility.

This study tests nasal application of nafamostat mesylate in liposomes to reduce SARS-CoV-2 viral load in hamsters, finding reduced nasal titer but no improvement in disease severity.

The paper shows that a single DNA double-strand break can trigger a checkpoint response that delays cell cycle progression, and its abrogation leads to micronucleated daughter cells.

The paper characterizes inhibitor resistance in Mps1 mutants using biophysical assays and crystal structures, showing that Cpd-5 is better tolerated than NMS-P715 in resistant mutants.