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D898_E901 RET Deletion Is Oncogenic, Responds to Selpercatinib, and Treatment Resistance Can Arise Via RET-Independent Mechanisms.

Tommaso PorcelliMarialuisa MocciaMaria Angela De StefanoRaffaele AmbrosioEttore CapoluongoMassimo SantoroJulien HadouxMartin SchlumbergerFrancesca CarlomagnoDomenico Salvatore
Published in: JCO precision oncology (2023)
deletion is a gain-of-function mutation and responds to tyrosine kinase inhibitors in MTC. RET Δ898-901 mutant is sensitive to selpercatinib and vandetanib, and acquired resistance to selpercatinib may develop via RET-independent mechanisms.
Keyphrases
  • transcription factor
  • combination therapy