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Please use this identifier to cite or link to this item: http://hdl.handle.net/1843/83923
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dc.creatorBruna Pizziolocourapt_BR
dc.creatorAline Carvalho Batistapt_BR
dc.creatorMarina Gonçalves Dinizpt_BR
dc.creatorRicardo Santiago Gomezpt_BR
dc.creatorSílvia Ferreira de Sousapt_BR
dc.creatorVanessa de Fátima Bernardespt_BR
dc.creatorJosiane Alves Françapt_BR
dc.creatorHelder Antonio Rebelo Pontespt_BR
dc.creatorDanyel Elias da Cruz Perezpt_BR
dc.creatorCarolina Cavaliéri Gomespt_BR
dc.creatorRicardo Luiz Cavalcanti de Albuquerque Juniorpt_BR
dc.creatorManoela Domingues Martinspt_BR
dc.date.accessioned2025-07-29T18:19:31Z-
dc.date.available2025-07-29T18:19:31Z-
dc.date.issued2019-07-
dc.citation.volume128pt_BR
dc.citation.issue1pt_BR
dc.citation.spagee77pt_BR
dc.citation.epagee77pt_BR
dc.identifier.issn2212-4411pt_BR
dc.identifier.urihttp://hdl.handle.net/1843/83923-
dc.description.resumoObjective: KRAS is the most frequently mutated onco gene in human neoplasms and we have previously reported KRAS p.G12V mutations in adenomatoid odontogenic tumors (AOT). We aimed to expand this cohort of samples and to test the association of KRAS mutations with clinical and histopatho logical parameters. A convenience sample of 30 AOT cases was included in the study. The hotpot KRAS p.G12V mutation was assessed by TaqMan allele-specific qPCR and codon 12 was direct sequenced. Clinical information obtained included patients age, tumor site, association of the lesion with impacted teeth and clinical tumor size. In addition, tumor capsule thickness was evaluated by morphometric analysis. Statistical analysis was car ried out to test the association of KRAS codon 12 mutations with clinico-pathological parameters. Findings: Molecular results confirmed KRAS p.G12V mutation in 14/23 cases, and p.G12R in 1/23. Eight cases were wild-type and samples from 7 cases failed amplification. Codon 12 mutations were not associated with any of the clinicopatho logical parameters tested (p>0.05). Conclusion: AOTshow high frequency of KRAS codon 12 mutations (15/23, 65%), which occur irrespectively of patients’ age, tumor location, association with impacted teeth, tumor clinical size or histopathological capsule thickness.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.format.mimetypepdfpt_BR
dc.languageengpt_BR
dc.publisherUniversidade Federal de Minas Geraispt_BR
dc.publisher.countryBrasilpt_BR
dc.publisher.departmentFAO - DEPARTAMENTO DE CLÍNICApt_BR
dc.publisher.departmentICB - DEPARTAMENTO DE PATOLOGIApt_BR
dc.publisher.initialsUFMGpt_BR
dc.relation.ispartofOral Surgery, Oral Medicine, Oral Pathology and Oral Radiologypt_BR
dc.rightsAcesso Restritopt_BR
dc.subject.otherAssociationpt_BR
dc.subject.otherMutationpt_BR
dc.subject.otherCodonpt_BR
dc.subject.otherOncogenespt_BR
dc.subject.otherEvaluation studypt_BR
dc.titleKRAS mutations drive adenomatoid odontogenic tumorpt_BR
dc.typeArtigo de Periódicopt_BR
dc.url.externahttps://www.oooojournal.net/article/S2212-4403(19)30327-X/fulltextpt_BR
dc.identifier.orcidhttps://orcid.org/0000-0002-9987-5311pt_BR
dc.identifier.orcidhttps://orcid.org/0000-0002-2117-5593pt_BR
dc.identifier.orcidhttps://orcid.org/0000-0002-4212-1172pt_BR
dc.identifier.orcidhttps://orcid.org/0000-0001-8770-8009pt_BR
dc.identifier.orcidhttps://orcid.org/0000-0001-7820-4749pt_BR
dc.identifier.orcidhttps://orcid.org/0000-0003-0194-7434pt_BR
dc.identifier.orcidhttps://orcid.org/0000-0002-6005-783Xpt_BR
dc.identifier.orcidhttps://orcid.org/0000-0002-7609-8804pt_BR
dc.identifier.orcidhttps://orcid.org/0000-0002-4591-4645pt_BR
dc.identifier.orcidhttps://orcid.org/0000-0003-1580-4995pt_BR
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