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Carcinogenic Ability of Schistosoma Haematobium Possibly through Oncogenic Mutation of KRAS Gene

dc.contributor.authorBotelho, Mónica C.
dc.contributor.authorVeiga, Isabel
dc.contributor.authorOliveira, Paula A.
dc.contributor.authorLopes, Carlos
dc.contributor.authorTeixeira, Manuel
dc.contributor.authorCosta, José M Correia da
dc.contributor.authorMachado, José C.
dc.date.accessioned2013-05-24T16:48:12Z
dc.date.available2013-05-24T16:48:12Z
dc.date.issued2013-04-28
dc.description.abstractSchistosoma haematobium is a parasitic flatworm that infects millions of people, mostly in the developing world, and is associated with high incidence of bladder cancer, although why is not clear. Previously, we have used CD-1 mice to show that Schistosoma haematobium total antigen (Sh) has a carcinogenic ability. Sh intravesically instillation induced the development of several urothelial lesions, namely nodular hyperplasia and dysplasia (LGIUN—Low Grade Intra-Urothelial Neoplasia) after 40 weeks of treatment. These results suggested that Sh induce urothelium malignization. Bladder carcinoma frequently harbours gene mutations that constitutively activate the receptor tyrosine kinase-Ras pathway for this reason we studied activating mutations in KRAS gene. Twenty percent of the bladders with dysplasia presented a KRAS mutation in codon 12 of exon 2. We concluded from these results that the parasite extract of S. haematobium has carcinogenic ability possibly through oncogenic mutation of KRAS gene.por
dc.identifier.citationAdvances in Cancer: Research & Treatment. 2013(2013):8 pag.por
dc.identifier.issn2326-702X
dc.identifier.otherdoi:10.5171/2013.876585
dc.identifier.urihttp://hdl.handle.net/10400.18/1581
dc.language.isoengpor
dc.publisherIBIMA Publishingpor
dc.relation.publisherversionhttp://www.ibimapublishing.com/journals/ACRT/2013/876585/876585.pdfpor
dc.subjectSchistosoma Haematobiumpor
dc.subjectBladder Cancerpor
dc.subjectOncogenespor
dc.subjectKras Mutationpor
dc.titleCarcinogenic Ability of Schistosoma Haematobium Possibly through Oncogenic Mutation of KRAS Genepor
dc.typejournal article
dspace.entity.typePublication
oaire.citation.endPage8por
oaire.citation.startPage1por
oaire.citation.volume2013por
rcaap.rightsopenAccesspor
rcaap.typearticlepor

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