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.

Anti-targets are proteins that cause problems when inhibited along with an intended target and our novel chemical strategy affords unprecedented selectivity in the context of FLT3 vs. KIT inhibition for treatment of a devastating blood cancer.

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.

The elongation rate of RNA Polymerase II varies greatly between and along genes, as this enzyme accelerates from stable pausing to rapid elongation within genes, and is influenced by CG-content, exons and chromatin.

An auxiliary subunit alters the effect of a family of small-molecule openers on a voltage-gated potassium channel by inducing structural re-arrangements that promote protonation of the drug molecule.

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.