De novo AML exhibits greater microenvironment dysregulation compared to AML with myelodysplasia-related changes

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dc.citation.volume7
dc.contributor.authorLopes, Matheus Rodrigues
dc.contributor.authorNovais Pereira, Joao Kleber
dc.contributor.authorCampos, Paula de Melo
dc.contributor.authorMachado-Neto, Joao Agostinho
dc.contributor.authorTraina, Fabiola
dc.contributor.authorOlalla Saad, Sara T.
dc.contributor.authorFavaro, Patricia [UNIFESP]
dc.coverageLondon
dc.date.accessioned2020-07-17T14:03:15Z
dc.date.available2020-07-17T14:03:15Z
dc.date.issued2017
dc.description.abstractThe interaction between the bone marrow microenvironment and malignant hematopoietic cells can result in the protection of leukemia cells from chemotherapy in both myelodysplastic syndromes (MDS) and acute myeloid leukemia (AML). We, herein, characterized the changes in cytokine expression and the function of mesenchymal stromal cells (MSC) in patients with MDS, AML with myelodysplasia-related changes (MRC), a well-recognized clinical subtype of secondary AML, and de novo AML. We observed a significant inhibitory effect of MDS-MSC on T-lymphocyte proliferation and no significant differences in any of the cytokines tested. AML-MSC inhibited T-cell proliferation only at a very low MSC/T cell ratio. When compared to the control, AML-MRC-derived MSC presented a significant increase in IL6 expression, whereas de novo AML MSC presented a significant increase in the expression levels of VEGFA, CXCL12, RPGE2, IDO, IL1 beta, IL6 and IL32, followed by a decrease in IL10 expression. Furthermore, data indicate that IL-32 regulates stromal cell proliferation, has a chemotactic potential and participates in stromal cell crosstalk with leukemia cells, which could result in chemoresistance. Our results suggest that the differences between AML-MRC and de novo AML also extend into the leukemic stem cell niche and that IL-32 can participate in the regulation of the bone marrow cytokine milieu.en
dc.description.affiliationUniv Estadual Campinas, Hematol & Transfus Med Ctr, Hemoctr Unicamp, Inst Nacl Ciencia & Tecnol Sangue, Sao Paulo, Brazil
dc.description.affiliationUniv Sao Paulo, Ribeirao Preto Med Sch, Dept Internal Med, Sao Paulo, Brazil
dc.description.affiliationUniv Fed Sao Paulo, Dept Biol Sci, Sao Paulo, Brazil
dc.description.affiliationFed Univ Vale do Sao Francisco, Paulo Afonso, BA, Brazil
dc.description.affiliationUnifespUniv Fed Sao Paulo, Dept Biol Sci, Sao Paulo, Brazil
dc.description.sourceWeb of Science
dc.description.sponsorshipConselho Nacional de Desenvolvimento Cientifico e Tecnologico (CNPq)
dc.description.sponsorshipFundacao de Amparo a Pesquisa do Estado de Sao Paulo (FAPESP)
dc.format.extent-
dc.identifierhttp://dx.doi.org/10.1038/srep40707
dc.identifier.citationScientific Reports. London, v. 7, p. -, 2017.
dc.identifier.doi10.1038/srep40707
dc.identifier.fileWOS000391927200001.pdf
dc.identifier.issn2045-2322
dc.identifier.urihttps://repositorio.unifesp.br/handle/11600/55258
dc.identifier.wosWOS:000391927200001
dc.language.isoeng
dc.publisherNature Publishing Group
dc.relation.ispartofScientific Reports
dc.rightsinfo:eu-repo/semantics/openAccess
dc.titleDe novo AML exhibits greater microenvironment dysregulation compared to AML with myelodysplasia-related changesen
dc.typeinfo:eu-repo/semantics/article
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