Abstract
Lineage plasticity facilitates therapeutic resistance in multiple cancers. In lung adenocarcinomas (LUADs), this phenomenon includes small cell and squamous cell (LUSC) histologic transdifferentiation in the context of acquired resistance to targeted inhibition of driver mutations. The incidence of LUSC transdifferentiation in EGFR mutant tumors occurs in up to 9% of cases relapsed on osimertinib and has been associated to poor prognosis. The paucity of well annotated pre- and post-transdifferentiation clinical samples has precluded the performance of informative molecular analyses: little is known about the molecular mechanisms leading to this histological transition.
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