Val600Glu (V600E) mutation is the most common BRAF mutation detected in thyroid cancer. Hence, recent research efforts have been performed trying to explore several inhibitors of the V600E mutation-containing BRAF kinase as potential therapeutic options in thyroid cancer refractory to standard interventions. Among them, vemurafenib is a selective BRAF inhibitor approved by FDA for clinical practice. Unfortunately, vemurafenib often displays limited efficacy in poorly differentiated and anaplastic thyroid carcinomas probably because of intrinsic and/or acquired resistance mechanisms. In this view, cancer stem cells may represent a possible mechanism of resistance to vemurafenib, due to their self-renewal and chemo resistance properties.

Computational modeling reveals MAP3K8 as mediator of resistance to vemurafenib in thyroid cancer stem cells

Pennisi, Marzio;
2019-01-01

Abstract

Val600Glu (V600E) mutation is the most common BRAF mutation detected in thyroid cancer. Hence, recent research efforts have been performed trying to explore several inhibitors of the V600E mutation-containing BRAF kinase as potential therapeutic options in thyroid cancer refractory to standard interventions. Among them, vemurafenib is a selective BRAF inhibitor approved by FDA for clinical practice. Unfortunately, vemurafenib often displays limited efficacy in poorly differentiated and anaplastic thyroid carcinomas probably because of intrinsic and/or acquired resistance mechanisms. In this view, cancer stem cells may represent a possible mechanism of resistance to vemurafenib, due to their self-renewal and chemo resistance properties.
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11579/114029
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