Targeted therapies induce an aberrant fucosylation of complex tumor secretomes stimulating the expansion of minority drug-resistant clones and promoting therapy resistance.

Genetically engineered murine models reveal novel mechanisms of cell identity regulation in lung cancer and provide insights into the complex interplay between lineage specifiers and oncogenic signaling pathways in this disease.

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.

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.

Loss of KEAP1 modulates sensitivity to targeted therapies in lung cancer.

RNF43 interacts with receptor complexes of the Wnt/PCP signaling and its enzymatic activity results in the reduced cells sensitivity to WNT5A what translates in melanoma into decreased invasive properties and increased response to targeted therapies of this skin cancer.

The packaging signal in HIV-1 genomic RNA supports in vitro particle assembly more efficiently than control RNAs, probably explaining its selective packaging during virus assembly in vivo.

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