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Factors that may influence polymorphous low-grade adenocarcinoma growth

dc.contributor.authorSoares, Andresa Borges
dc.contributor.authorMartinez, Elizabeth Ferreira
dc.contributor.authorAvila Ribeiro, Patricia Fernandes
dc.contributor.authorBarreto, Icleia Siqueira
dc.contributor.authorAguiar, Maria Cassia
dc.contributor.authorFuruse, Cristiane [UNESP]
dc.contributor.authorSperandio, Marcelo
dc.contributor.authorMontalli, Victor Angelo
dc.contributor.authorAraujo, Ney Soares de
dc.contributor.authorAraujo, Vera Cavalcanti de
dc.contributor.institutionSao Leopoldo Mandic Inst & Res Ctr
dc.contributor.institutionUniversidade Federal de Minas Gerais (UFMG)
dc.contributor.institutionUniversidade Estadual Paulista (Unesp)
dc.date.accessioned2018-11-26T17:24:28Z
dc.date.available2018-11-26T17:24:28Z
dc.date.issued2017-04-01
dc.description.abstractThere is mounting evidence on the importance of some biological processes in tumor growth, such as vascular supply, apoptosis, autophagy, and senescence. We have investigated these processes in polymorphous low-grade adenocarcinoma (PLGA), in an attempt to identify those that are relevant for this particular lesion. We analyzed 31 cases of PLGA using immunohistochemistry to antibodies against CD34 and CD105 to detect blood vessels; against D2-40 to detect lymphatic vessels; against Bax, Bcl-2, and survivin to explore cell apoptosis; and against Beclin and LCB3 to investigate autophagy and against p21 and p16 to assess senescence. Our results showed that PLGA growth does not depend on newly formed vessels but only on preexisting vasculature. Furthermore, PLGA is promoted by autophagy, sustained by both anti-apoptotic and anti-senescence signals, and stimulated by Bcl-2 and survivin.en
dc.description.affiliationSao Leopoldo Mandic Inst & Res Ctr, Dept Oral Pathol, Rua Jose Rocha Junqueira,13 Ponte Preta, BR-13045755 Campinas, SP, Brazil
dc.description.affiliationUniv Fed Minas Gerais, Dept Oral Pathol, Belo Horizonte, MG, Brazil
dc.description.affiliationState Univ Sao Paulo, Dept Oral Pathol, Aracatuba, SP, Brazil
dc.description.affiliationUnespState Univ Sao Paulo, Dept Oral Pathol, Aracatuba, SP, Brazil
dc.description.sponsorshipFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
dc.description.sponsorshipConselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
dc.description.sponsorshipIdFAPESP: 2015/12418-5
dc.description.sponsorshipIdCNPq: 304031/2014-3
dc.format.extent437-443
dc.identifierhttp://dx.doi.org/10.1007/s00428-017-2085-3
dc.identifier.citationVirchows Archiv. New York: Springer, v. 470, n. 4, p. 437-443, 2017.
dc.identifier.doi10.1007/s00428-017-2085-3
dc.identifier.fileWOS000399037800010.pdf
dc.identifier.issn0945-6317
dc.identifier.lattes1622189974684508
dc.identifier.orcid0000-0002-1330-1983
dc.identifier.urihttp://hdl.handle.net/11449/162691
dc.identifier.wosWOS:000399037800010
dc.language.isoeng
dc.publisherSpringer
dc.relation.ispartofVirchows Archiv
dc.relation.ispartofsjr1,207
dc.rights.accessRightsAcesso aberto
dc.sourceWeb of Science
dc.subjectPolymorphous low-grade adenocarcinoma
dc.subjectAngiogenesis
dc.subjectApoptosis
dc.subjectAutophagy
dc.subjectSenescence
dc.subjectBcl2
dc.subjectSurvivin
dc.subjectLC3B
dc.titleFactors that may influence polymorphous low-grade adenocarcinoma growthen
dc.typeArtigo
dcterms.licensehttp://www.springer.com/open+access/authors+rights?SGWID=0-176704-12-683201-0
dcterms.rightsHolderSpringer
unesp.author.lattes1622189974684508[6]
unesp.author.orcid0000-0002-1330-1983[6]
unesp.campusUniversidade Estadual Paulista (Unesp), Faculdade de Odontologia, Araçatubapt
unesp.departmentPatologia e Propedêutica Clínica - FOApt

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