Anticancer compound library screen identified many types of nucleolar stress and revealed an essential role of transcriptional cyclin-dependent kinases in nucleolar structure and function.

Combined analyses of transcriptome and chromatin accessibility elucidated the mechanisms underlying cancer cell lines response to antitumor candidates and provided a versatile perturbation-informed basal signature able to predict drug sensitivity.

Studies of the substrate selectivity of concentrative nucleoside transporters provide proof of principle for structure-based improvement of drug delivery by these transporters.

NICEdrug.ch is a resource allowing systematic and large-scale computational analysis of drug biochemistry, enzymatic targets, and toxicity in the context of cellular metabolism.

Stimulation of the rate-limiting enzyme in the NAD salvage pathway protected against neurotoxicity and subsequent peripheral neuropathy associated with the widely utilized anticancer drug, paclitaxel.

An unbiased genetic screen in human cells shows that the molecular target of a natural product with promising anticancer activity is a membrane phospholipid.

A new zebrafish study identifies compounds that shield ears and kidneys against an anticancer drug.

Mutations conferring resistance to Escherichia coli against the chemotherapy drug gemcitabine can have opposite effects on bacterial drug degradation and therefore can increase or decrease the chemotherapy load on neighboring cancer cells.

The dimer destabilizers cause a dimer-to-monomer equilibrium shift favoring the human thymidylate synthase monomer more degradable by the proteasome, thus breaking the long-standing link between inhibition and enhanced expression of the protein to fight cancer drug resistance.