KRAS resistance in cancer treatment
KRAS mutations drive some of the most aggressive cancers, but even the most promising therapies face a major hurdle: resistance. Tumor cells can survive treatment by entering a reversible “drug-tolerant persister” state, eventually acquiring permanent genetic changes that render therapy ineffective. Understanding this journey from persistence to resistance is critical for developing strategies that prevent treatment failure.
Download the poster to discover:
- How HUB Organoids faithfully recapitulate patient tumors, making them ideal for studying resistance
- How we generated persistent and resistant PDO models using stepwise drug exposure and dose escalation
- Whole exome sequencing data revealing KRAS-pathway mutations unique to resistant models
- Transcriptomic profiles showing distinct resistant-specific expression patterns, including downregulation of drug transporter pumps
Learn how our KRASmut organoid screen enables efficient testing of inhibitors and combination therapies
