A study that models the evolution of drug resistance in tumors reveals that drugs are more effective when given in combination than sequentially, and that cure is much more likely when the drugs target different pathways.

Targeting the activation of the androgen receptor N-terminal domain by the cochaperone Bag-1L provides a new approach for inhibiting androgen receptor function to treat prostate cancer.

Libraries of patient-derived tumor organoids are a reliable and scalable model system that can help identify and optimize targeted therapies in a pre-clinical setting.

Maternal embryonic leucine zipper kinase (MELK) is a new anti-cancer target that is highly selective for basal-like breast cancer.

SOX2 causes resistance to anti-EGFR therapies in EGFR-mutant lung cancer.

Systematic analyses of natural variants and artificial mutants establish functional landscapes of BRCA1 for homology-directed repair (HDR) and therapy resistance and identify the BRCA1-PALB2 interaction as a key control point for HDR pathway choice.

A geneome-scale shRNA screen identifies five genes whose suppression promotes cell death upon PI3K inhibition both in vitro and in vivo, thus suggesting potential combination therapies involving PI3K inhibition.

The nodes of the cytosolic proteostasis network can control sensitivity to proteasome inhibitors and decreased levels of the 19S proteasomal regulator can lead to increased resistance to inhibitors.

A drug used in hormone replacement therapy can target estrogen receptors that have become resistant to breast cancer treatments.