Reliance upon ancestral mutations is maintained in colorectal cancers that heterogeneously evolve during targeted therapies

Abstract

The emergence of sub-clones that are resistant to targeted agents is a major therapeutic obstacle in oncology. Here, using colorectal cancer as a model system, the authors show that interfering with ancestral oncogenic events present in all subclones-like APC-WNT pathway alterations—can restrain the emergence of drug-resistant populations.