Tenzin Kungyal

This study identifies the CD109-SMURF2 axis as a mechanism that prevents EGFR degradation, sustaining oncogenic signaling and promoting SCC invasion and stemness.

This study shows that soluble CD109 inhibits EGFR signaling and cancer stemness in HNSCC by blocking mCD109-EGFR interactions and promoting EGFR degradation.

This study examines EGFR mutation subtypes in lung cancer, finding distinct metabolic profiles and clinical outcomes, with T790M mutations linked to poorer survival and metabolic reprogramming.