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

Fiorenza Gianì; Giulia Russo; MARZIO ALFIO PENNISI; Laura Sciacca; Francesco Frasca; Francesco Pappalardo

doi:10.1093/bioinformatics/bty969

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

Fiorenza Gianì, Giulia Russo, MARZIO ALFIO PENNISI, Laura Sciacca, Francesco Frasca, Francesco Pappalardo

Dipartimento di Scienze e Innovazione Tecnologica

Risultato della ricerca: Contributo su rivista › Articolo in rivista › peer review

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.

Lingua originale	Inglese
pagine (da-a)	2267-2275
Numero di pagine	9
Rivista	Bioinformatics
Volume	35
Numero di pubblicazione	13
DOI	https://doi.org/10.1093/bioinformatics/bty969
Stato di pubblicazione	Pubblicato - 2019

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10.1093/bioinformatics/bty969

http://hdl.handle.net/11579/114029

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title = "Computational modeling reveals MAP3K8 as mediator of resistance to vemurafenib in thyroid cancer stem cells",

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.",

author = "Fiorenza Gian{\`i} and Giulia Russo and PENNISI, {MARZIO ALFIO} and Laura Sciacca and Francesco Frasca and Francesco Pappalardo",

year = "2019",

doi = "10.1093/bioinformatics/bty969",

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T1 - Computational modeling reveals MAP3K8 as mediator of resistance to vemurafenib in thyroid cancer stem cells

AU - Gianì, Fiorenza

AU - Russo, Giulia

AU - PENNISI, MARZIO ALFIO

AU - Sciacca, Laura

AU - Frasca, Francesco

AU - Pappalardo, Francesco

PY - 2019

Y1 - 2019

N2 - 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.

AB - 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.

UR - https://iris.uniupo.it/handle/11579/114029

U2 - 10.1093/bioinformatics/bty969

DO - 10.1093/bioinformatics/bty969

M3 - Article

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VL - 35

SP - 2267

EP - 2275

JO - Bioinformatics

JF - Bioinformatics

IS - 13

ER -

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

Abstract

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