Reprogramming paneth-like plasticity: FGFR3 as a key to overcoming KRAS-EGFR resistance in CRC

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Figure 1.
Schematic representation of CRC cell plasticity in resistance to dual KRAS and EGFR inhibition. Dual inhibition of KRAS and EGFR induces resistance in CRC via Paneth-like transdifferentiation of CRC cells (top right). Non-classic SMAD1 signaling activation drives Paneth-like lineage plasticity through upregulation of FGFR3 and its ligands, and FGFR3 blockade reverses resistance to KRAS and EGFR dual inhibition in CRC (bottom-left).