TRPV4 and KRAS and FGFR1 gain-of-function mutations drive giant cell lesions of the jaw

Giant cell lesions of the jaw (GCLJ) are debilitating benign tumors of unclear origin. The authors identify driver recurrent somatic mutations in TRPV4, KRAS and FGFR1 and show they converge on aberrant activation of the MAPK pathway. Their findings extend the spectrum of TRPV4 channelopathies and p...

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Autores principales:	Carolina Cavalieri Gomes, Tenzin Gayden, Andrea Bajic, Osama F. Harraz, Jonathan Pratt, Hamid Nikbakht, Eric Bareke, Marina Gonçalves Diniz, Wagner Henriques Castro, Pascal St-Onge, Daniel Sinnett, HyeRim Han, Barbara Rivera, Leonie G. Mikael, Nicolas De Jay, Claudia L. Kleinman, Elvis Terci Valera, Angelia V. Bassenden, Albert M. Berghuis, Jacek Majewski, Mark T. Nelson, Ricardo Santiago Gomez, Nada Jabado
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2018
Materias:	Science Q
Acceso en línea:	https://doaj.org/article/e7587955769c46cb9c57d9d348d2db3d
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spelling	oai:doaj.org-article:e7587955769c46cb9c57d9d348d2db3d2021-12-02T17:33:03ZTRPV4 and KRAS and FGFR1 gain-of-function mutations drive giant cell lesions of the jaw10.1038/s41467-018-06690-42041-1723https://doaj.org/article/e7587955769c46cb9c57d9d348d2db3d2018-11-01T00:00:00Zhttps://doi.org/10.1038/s41467-018-06690-4https://doaj.org/toc/2041-1723Giant cell lesions of the jaw (GCLJ) are debilitating benign tumors of unclear origin. The authors identify driver recurrent somatic mutations in TRPV4, KRAS and FGFR1 and show they converge on aberrant activation of the MAPK pathway. Their findings extend the spectrum of TRPV4 channelopathies and provide rationale for targeted therapies at the bedside in GCLJ.Carolina Cavalieri GomesTenzin GaydenAndrea BajicOsama F. HarrazJonathan PrattHamid NikbakhtEric BarekeMarina Gonçalves DinizWagner Henriques CastroPascal St-OngeDaniel SinnettHyeRim HanBarbara RiveraLeonie G. MikaelNicolas De JayClaudia L. KleinmanElvis Terci ValeraAngelia V. BassendenAlbert M. BerghuisJacek MajewskiMark T. NelsonRicardo Santiago GomezNada JabadoNature PortfolioarticleScienceQENNature Communications, Vol 9, Iss 1, Pp 1-8 (2018)
institution	DOAJ
collection	DOAJ
language	EN
topic	Science Q
spellingShingle	Science Q Carolina Cavalieri Gomes Tenzin Gayden Andrea Bajic Osama F. Harraz Jonathan Pratt Hamid Nikbakht Eric Bareke Marina Gonçalves Diniz Wagner Henriques Castro Pascal St-Onge Daniel Sinnett HyeRim Han Barbara Rivera Leonie G. Mikael Nicolas De Jay Claudia L. Kleinman Elvis Terci Valera Angelia V. Bassenden Albert M. Berghuis Jacek Majewski Mark T. Nelson Ricardo Santiago Gomez Nada Jabado TRPV4 and KRAS and FGFR1 gain-of-function mutations drive giant cell lesions of the jaw
description	Giant cell lesions of the jaw (GCLJ) are debilitating benign tumors of unclear origin. The authors identify driver recurrent somatic mutations in TRPV4, KRAS and FGFR1 and show they converge on aberrant activation of the MAPK pathway. Their findings extend the spectrum of TRPV4 channelopathies and provide rationale for targeted therapies at the bedside in GCLJ.
format	article
author	Carolina Cavalieri Gomes Tenzin Gayden Andrea Bajic Osama F. Harraz Jonathan Pratt Hamid Nikbakht Eric Bareke Marina Gonçalves Diniz Wagner Henriques Castro Pascal St-Onge Daniel Sinnett HyeRim Han Barbara Rivera Leonie G. Mikael Nicolas De Jay Claudia L. Kleinman Elvis Terci Valera Angelia V. Bassenden Albert M. Berghuis Jacek Majewski Mark T. Nelson Ricardo Santiago Gomez Nada Jabado
author_facet	Carolina Cavalieri Gomes Tenzin Gayden Andrea Bajic Osama F. Harraz Jonathan Pratt Hamid Nikbakht Eric Bareke Marina Gonçalves Diniz Wagner Henriques Castro Pascal St-Onge Daniel Sinnett HyeRim Han Barbara Rivera Leonie G. Mikael Nicolas De Jay Claudia L. Kleinman Elvis Terci Valera Angelia V. Bassenden Albert M. Berghuis Jacek Majewski Mark T. Nelson Ricardo Santiago Gomez Nada Jabado
author_sort	Carolina Cavalieri Gomes
title	TRPV4 and KRAS and FGFR1 gain-of-function mutations drive giant cell lesions of the jaw
title_short	TRPV4 and KRAS and FGFR1 gain-of-function mutations drive giant cell lesions of the jaw
title_full	TRPV4 and KRAS and FGFR1 gain-of-function mutations drive giant cell lesions of the jaw
title_fullStr	TRPV4 and KRAS and FGFR1 gain-of-function mutations drive giant cell lesions of the jaw
title_full_unstemmed	TRPV4 and KRAS and FGFR1 gain-of-function mutations drive giant cell lesions of the jaw
title_sort	trpv4 and kras and fgfr1 gain-of-function mutations drive giant cell lesions of the jaw
publisher	Nature Portfolio
publishDate	2018
url	https://doaj.org/article/e7587955769c46cb9c57d9d348d2db3d
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TRPV4 and KRAS and FGFR1 gain-of-function mutations drive giant cell lesions of the jaw

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