Bandrés Elizalde, Eva
Loading...
Email Address
person.page.identifierURI
Birth Date
Job Title
Last Name
Bandrés Elizalde
First Name
Eva
person.page.departamento
Ciencias de la Salud
person.page.instituteName
ORCID
person.page.observainves
person.page.upna
Name
- Publications
- item.page.relationships.isAdvisorOfPublication
- item.page.relationships.isAdvisorTFEOfPublication
- item.page.relationships.isAuthorMDOfPublication
2 results
Search Results
Now showing 1 - 2 of 2
Publication Open Access Assessment of minimal residual disease by next generation sequencing in peripheral blood as a complementary tool for personalized transplant monitoring in myeloid neoplasms(MDPI, 2020) Aguirre-Ruiz, Paula; Ariceta, Beñat; Viguria Alegría, María Cruz; Zudaire, María Teresa; Blasco-Iturri, Zuriñe; Arnedo, Patricia; Aguilera-Diaz, Almudena; Jauregui, Axier; Mañú, Amagoia; Prósper, Felipe; Mateos, María Carmen; Fernández-Mercado, Marta; Larráyoz, María José; Redondo, Margarita; Calasanz, María José; Bandrés Elizalde, Eva; Vázquez Urio, Iria; Ciencias de la Salud; Osasun Zientziak; Gobierno de Navarra / Nafarroako GobernuaPatients with myeloid neoplasms who relapsed after allogenic hematopoietic stem cell transplant (HSCT) have poor prognosis. Monitoring of chimerism and specific molecular markers as a surrogate measure of relapse is not always helpful; therefore, improved systems to detect early relapse are needed. We hypothesized that the use of next generation sequencing (NGS) could be a suitable approach for personalized follow-up post-HSCT. To validate our hypothesis, we analyzed by NGS, a retrospective set of peripheral blood (PB) DNA samples previously evaluated by high-sensitive quantitative PCR analysis using insertion/deletion polymorphisms (indel-qPCR) chimerism engraftment. Post-HCST allelic burdens assessed by NGS and chimerism status showed a similar time-course pattern. At time of clinical relapse in 8/12 patients, we detected positive NGS-based minimal residual disease (NGS-MRD). Importantly, in 6/8 patients, we were able to detect NGS-MRD at time points collected prior to clinical relapse. We also confirmed the disappearance of post-HCST allelic burden in non-relapsed patients, indicating true clinical specificity. This study highlights the clinical utility of NGS-based post-HCST monitoring in myeloid neoplasia as a complementary specific analysis to high-sensitive engraftment testing. Overall, NGS-MRD testing in PB is widely applicable for the evaluation of patients following HSCT and highly valuable to personalized early treatment intervention when mixed chimerism is detected.Publication Open Access EVI1 controls proliferation in acute myeloid leukaemia through modulation of miR-1-2(Nature Publishing Group, 2010-09-14) Gómez-Benito, María; Conchillo, Ana; García, M. A.; Vázquez Urio, Iria; Maicas, Miren; Vicente, Carmen; Cristobal, I.; Marcotegui, Nerea; García-Ortí, L.; Bandrés Elizalde, Eva; Calasanz, María José ; Alonso, M. M.; Odero, María D.; Ciencias; Zientziak; Ciencias de la Salud; Osasun Zientziak; Gobierno de Navarra / Nafarroako GobernuaBakground: the EVI1(ecotropic virus integration site 1) gene codes for a zinc-finger transcription factor, whose transcriptional activation leads to a particularly aggressive form of acute myeloid leukaemia (AML). Although, EVI1 interactions with key proteins in hematopoiesis have been previously described, the precise role of this transcription factor in promoting leukaemic transformation is not completely understood. Recent works have identified specific microRNA (miRNA) signatures in different AML subgroups. However, there is no analysis of miRNAs profiles associated with EVI1 overexpression in humans. Methods: we performed QT-RT-PCR to assess the expression of 250 miRNAs in cell lines with or without EVI1 overexpression and in patient samples. We used ChIP assays to evaluated the possible binding of EVI1 binding to the putative miRNA promoter. Proliferation of the different cell lines transfected with the anti- or pre-miRs was quantified by MTT. Results: our data showed that EVI1 expression was significantly correlated with the expression of miR-1-2 and miR-133-a-1 in established cell lines and in patient samples. ChIP assays confirmed that EVI1 binds directly to the promoter of these two miRNAs. However, only miR-1-2 was involved in abnormal proliferation in EVI1 expressing cell lines. Conclusions: our data showed that EVI1 controls proliferation in AML through modulation of miR-1-2. This study contributes to further understand the transcriptional networks involving transcription factors and miRNAs in AML.