Antifibrotic drugs as therapeutic tools in resistant melanoma

Melanoma is the most aggressive form of skin cancer. Together with the recent advances in immunotherapy, targeted therapy with inhibitors of the Mitogen Activated Protein Kinase (MAPKi) pathway including BRAF and MEK inhibitors has greatly improved the clinical outcome of these patients. Unfortunate...

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Main Authors: Berta Sanchez‐Laorden, M Angela Nieto
Format: Article
Language:English
Published: Springer Nature 2022-03-01
Series:EMBO Molecular Medicine
Online Access:https://doi.org/10.15252/emmm.202115449
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author Berta Sanchez‐Laorden
M Angela Nieto
author_facet Berta Sanchez‐Laorden
M Angela Nieto
author_sort Berta Sanchez‐Laorden
collection DOAJ
description Melanoma is the most aggressive form of skin cancer. Together with the recent advances in immunotherapy, targeted therapy with inhibitors of the Mitogen Activated Protein Kinase (MAPKi) pathway including BRAF and MEK inhibitors has greatly improved the clinical outcome of these patients. Unfortunately, due to genetic and non‐genetic events, many patients develop resistance to MAPKi. Melanoma phenotypic plasticity, understood as the ability of melanoma cells to dynamically transition between different states with varying levels of differentiation/dedifferentiation, is key for melanoma progression. Lineage plasticity has also emerged as an important mechanism of non‐genetic adaptive melanoma drug resistance in the clinic (Arozarena & Wellbrock, 2019), highlighting the need for a deeper characterization of the mechanisms that control this process. In this issue of EMBO Molecular Medicine, Diazzi et al (2022) identify a mechanism regulating MAPKi‐induced phenotypic plasticity and resistance, providing evidence to support the use of an anti‐fibrotic drug as a potential novel combinatorial therapeutic approach.
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spelling doaj.art-d0823d698f464087b9286764f10582a22024-03-02T04:52:15ZengSpringer NatureEMBO Molecular Medicine1757-46761757-46842022-03-01143n/an/a10.15252/emmm.202115449Antifibrotic drugs as therapeutic tools in resistant melanomaBerta Sanchez‐Laorden0M Angela Nieto1Instituto de Neurociencias (CSIC‐UMH) Sant Joan d’Alacant SpainInstituto de Neurociencias (CSIC‐UMH) Sant Joan d’Alacant SpainMelanoma is the most aggressive form of skin cancer. Together with the recent advances in immunotherapy, targeted therapy with inhibitors of the Mitogen Activated Protein Kinase (MAPKi) pathway including BRAF and MEK inhibitors has greatly improved the clinical outcome of these patients. Unfortunately, due to genetic and non‐genetic events, many patients develop resistance to MAPKi. Melanoma phenotypic plasticity, understood as the ability of melanoma cells to dynamically transition between different states with varying levels of differentiation/dedifferentiation, is key for melanoma progression. Lineage plasticity has also emerged as an important mechanism of non‐genetic adaptive melanoma drug resistance in the clinic (Arozarena & Wellbrock, 2019), highlighting the need for a deeper characterization of the mechanisms that control this process. In this issue of EMBO Molecular Medicine, Diazzi et al (2022) identify a mechanism regulating MAPKi‐induced phenotypic plasticity and resistance, providing evidence to support the use of an anti‐fibrotic drug as a potential novel combinatorial therapeutic approach.https://doi.org/10.15252/emmm.202115449
spellingShingle Berta Sanchez‐Laorden
M Angela Nieto
Antifibrotic drugs as therapeutic tools in resistant melanoma
EMBO Molecular Medicine
title Antifibrotic drugs as therapeutic tools in resistant melanoma
title_full Antifibrotic drugs as therapeutic tools in resistant melanoma
title_fullStr Antifibrotic drugs as therapeutic tools in resistant melanoma
title_full_unstemmed Antifibrotic drugs as therapeutic tools in resistant melanoma
title_short Antifibrotic drugs as therapeutic tools in resistant melanoma
title_sort antifibrotic drugs as therapeutic tools in resistant melanoma
url https://doi.org/10.15252/emmm.202115449
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