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  3. Artigo de Periódico
Use este identificador para citar o ir al link de este elemento: http://hdl.handle.net/1843/60209
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Campo DCValorIdioma
dc.creatorJéssica Gardone Vitóriopt_BR
dc.creatorLiséte Celina Langept_BR
dc.creatorLucilaine Valéria de Souza Santospt_BR
dc.creatorMartin Røssel Larsenpt_BR
dc.creatorCarolina Cavalieri Gomespt_BR
dc.creatorRicardo Santiago Gomezpt_BR
dc.creatorFilipe Fideles Duarte-Andradept_BR
dc.creatorThais dos Santos Fontes Pereirapt_BR
dc.creatorMarcella Nunes de Melo Bragapt_BR
dc.creatorGisele André Baptista Canutopt_BR
dc.creatorAdriana Nori de Macedopt_BR
dc.creatorYuri Abner Rocha Lebronpt_BR
dc.creatorVictor Rezende Moreirapt_BR
dc.creatorLiza Figueiredo Felicoript_BR
dc.date.accessioned2023-10-27T22:06:54Z-
dc.date.available2023-10-27T22:06:54Z-
dc.date.issued2022-
dc.citation.volume51pt_BR
dc.citation.issue7pt_BR
dc.citation.spage666pt_BR
dc.citation.epage673pt_BR
dc.identifier.doihttps://doi.org/10.1111/jop.13327pt_BR
dc.identifier.issn0904-2512pt_BR
dc.identifier.urihttp://hdl.handle.net/1843/60209-
dc.description.resumoBackground: Giant cell granuloma of the jaws are benign osteolytic lesions of the jaws. These lesions are genetically characterized by mutually exclusive somatic mutations at TRPV4, KRAS, and FGFR1, and a fourth molecular subgroup which is wild-type for the three mutations. Irrespective of the molecular background, giant cell granulomas show MAPK/ERK activation. However, it remains unclear if these mutations lead to differences in their molecular signaling in giant cell granulomas. Methods: Metabolomics, proteomics, and phosphoproteomics analyses were carried out in formalin-fixed paraffin-embedded samples of giant cell granuloma of the jaws. The study cohort consisted of five lesions harboring mutations in FGFR1, six in KRAS, five in TRPV4, and five that were wild-type for these mutations. Results: Lesions harboring KRAS or FGFR1 mutations showed overall similar proteomics and metabolomics profiles. In all four groups, metabolic pathways showed similarity in apoptosis, cell signaling, gene expression, cell differentiation, and erythrocyte activity. Lesions harboring TRPV4 mutations showed a greater number of enriched pathways related to tissue architecture. On the other hand, the wild-type group presented increased number of enriched pathways related to protein metabolism compared to the other groups. Conclusion: Despite some minor differences, our results revealed an overall similar molecular profile among the groups with different mutational profile at the metabolic, proteic, and phosphopeptidic levels.pt_BR
dc.description.sponsorshipCNPq - Conselho Nacional de Desenvolvimento Científico e Tecnológicopt_BR
dc.description.sponsorshipFAPEMIG - Fundação de Amparo à Pesquisa do Estado de Minas Geraispt_BR
dc.description.sponsorshipCAPES - Coordenação de Aperfeiçoamento de Pessoal de Nível Superiorpt_BR
dc.description.sponsorshipOutra Agênciapt_BR
dc.languageengpt_BR
dc.publisherUniversidade Federal de Minas Geraispt_BR
dc.publisher.countryBrasilpt_BR
dc.publisher.departmentICB - DEPARTAMENTO DE BIOQUÍMICA E IMUNOLOGIApt_BR
dc.publisher.departmentICB - DEPARTAMENTO DE MORFOLOGIApt_BR
dc.publisher.departmentICB - DEPARTAMENTO DE PATOLOGIApt_BR
dc.publisher.departmentICX - DEPARTAMENTO DE QUÍMICApt_BR
dc.publisher.initialsUFMGpt_BR
dc.relation.ispartofJournal of Oral Pathology & Medicinept_BR
dc.rightsAcesso Restritopt_BR
dc.subjectLesão central de células gigantespt_BR
dc.subjectMetabolômicapt_BR
dc.subjectProteomapt_BR
dc.subjectBiologia molecularpt_BR
dc.subjectBiologia de tumorespt_BR
dc.subject.otherBiologia molecularpt_BR
dc.subject.otherCélulas - Patogênesept_BR
dc.subject.otherTumorespt_BR
dc.subject.otherPreparação de amostra (Química)pt_BR
dc.subject.otherGranulomapt_BR
dc.titleIntegrated proteomics, phosphoproteomics and metabolomics analyses reveal similarities among giant cell granulomas of the jaws with different genetic mutationspt_BR
dc.typeArtigo de Periódicopt_BR
dc.url.externahttps://onlinelibrary.wiley.com/doi/10.1111/jop.13327pt_BR
dc.identifier.orcidhttps://orcid.org/0000-0001-6203-0123pt_BR
dc.identifier.orcidhttps://orcid.org/0000-0002-4125-3755pt_BR
dc.identifier.orcidhttps://orcid.org/0000-0003-0345-0376pt_BR
dc.identifier.orcidhttps://orcid.org/0000-0002-6174-8157pt_BR
dc.identifier.orcidhttps://orcid.org/0000-0002-5009-6675pt_BR
dc.identifier.orcidhttps://orcid.org/0009-0004-4352-1460pt_BR
dc.identifier.orcidhttps://orcid.org/0000-0001-6933-8454pt_BR
dc.identifier.orcidhttps://orcid.org/0000-0002-6616-3705pt_BR
dc.identifier.orcidhttps://orcid.org/0000-0002-3240-9658pt_BR
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