De Novo Aml Exhibits Greater Microenvironment Dysregulation Compared To Aml With Myelodysplasia-related Changes

dc.creatorLopes
dc.creatorMatheus Rodrigues; Novais Pereira
dc.creatorJoao Kleber; Campos
dc.creatorPaula de Melo; Machado-Neto
dc.creatorJoao Agostinho; Traina
dc.creatorFabiola; Olalla Saad
dc.creatorSara T.; Favaro
dc.creatorPatricia
dc.date2017
dc.datejan
dc.date2017-11-13T13:44:08Z
dc.date2017-11-13T13:44:08Z
dc.date.accessioned2018-03-29T05:58:47Z
dc.date.available2018-03-29T05:58:47Z
dc.identifierScientific Reports. Nature Publishing Group, v. 7, p. , 2017.
dc.identifier2045-2322
dc.identifierWOS:000391927200001
dc.identifier10.1038/srep40707
dc.identifierhttp://www-nature.ez88.periodicos.capes.gov.br/articles/srep40707
dc.identifierhttp://repositorio.unicamp.br/jspui/handle/REPOSIP/328699
dc.identifier.urihttp://repositorioslatinoamericanos.uchile.cl/handle/2250/1365724
dc.descriptionConselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
dc.descriptionFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
dc.descriptionThe 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.
dc.description7
dc.descriptionConselho Nacional de Desenvolvimento Cientifico e Tecnologico (CNPq)
dc.descriptionFundacao de Amparo a Pesquisa do Estado de Sao Paulo (FAPESP)
dc.descriptionConselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
dc.descriptionFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
dc.languageEnglish
dc.publisherNature Publishing Group
dc.publisherLondon
dc.relationScientific Reports
dc.rightsaberto
dc.sourceWOS
dc.subjectAcute Myeloid-leukemia
dc.subjectMesenchymal Stromal Cells
dc.subjectNf-kappa-b
dc.subjectBone-marrow
dc.subjectStem-cells
dc.subjectT-cells
dc.subjectHematopoietic Progenitors
dc.subjectProinflammatory Cytokine
dc.subjectRheumatoid-arthritis
dc.subjectTnf-alpha
dc.titleDe Novo Aml Exhibits Greater Microenvironment Dysregulation Compared To Aml With Myelodysplasia-related Changes
dc.typeArtículos de revistas


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