ArticleEndocrine2026
Anti-tumour effects of combined lenvatinib and EGFR Inhibition in advanced differentiated thyroid cancer cells.
Article in Endocrine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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6 authors.
Funding
Abstract
purposeDifferentiated thyroid cancer (DTC) typically has a favourable prognosis, while advanced forms of these tumours exhibit aggressive behaviour, leading to decreased survival. Lenvatinib has demonstrated effectiveness in managing advanced DTC. However, its long-term efficacy is compromised by resistance mechanisms, which remain unexplored, limiting its clinical utility.
methodsIn vitro studies were conducted using three advanced DTC cell lines of the papillary subtype: K1 (BRAF p.V600E), BCPAP (BRAF p.V600E) and TPC-1 (RET/PTC1). IC50 for Lenvatinib and Gefitinib were defined, and their effects on cell viability, colony formation, gene expression, and pathway activation were assessed individually and in combination. Comparative genomic hybridisation was performed to uncover intrinsic resistance mechanisms.
resultsLenvatinib IC50 was higher in K1 and BCPAP than in TPC-1, indicating greater TPC-1 susceptibility, as confirmed by viability assays. Gefitinib showed similar IC50 values across all cell lines. The Lenvatinib plus Gefitinib combination (Combo) significantly reduced K1 and BCPAP viability when comparing with monotherapies, with no significant effects in TPC-1. Clonogenic assays mirrored these results and revealed higher recovery in K1 and BCPAP after Combo withdrawal. Combo treatment increased EGFR expression and induced ERK1/2 and AKT phosphorylation’s dysregulation in all cell lines.
conclusionsThis study showed that RET/PTC1 cells are more responsive to Lenvatinib than BRAF-mutated cells, and that EGFR targeting with Gefitinib enhanced Lenvatinib’s inhibitory effect in BRAF-mutated cells. Dysregulation of EGFR and Lenvatinib target gene’s expression, as well as of MAPK and PI3K signalling may indicate short-term adaptive resistance. These findings provide insight into Lenvatinib resistance mechanisms in thyroid cancer and highlight the need for further research to overcome refractoriness.
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