ESTELA MARIA NOVAK

(Fonte: Lattes)
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Instituto da Criança, Hospital das Clínicas, Faculdade de Medicina
LIM/36 - Laboratório de Pediatria Clínica, Hospital das Clínicas, Faculdade de Medicina
LIM/31 - Laboratório de Genética e Hematologia Molecular, Hospital das Clínicas, Faculdade de Medicina

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  • article 73 Citação(ões) na Scopus
    Synthesis, characterization and biological evaluation of Rutin-zinc(II) flavonoid -metal complex
    (2015) IKEDA, Norma Estefania Andrades; NOVAK, Estela Maria; MARIA, Durvanei Augusto; VELOSA, Adelia Segin; PEREIRA, Regina Mara Silva
    Synthesis of compounds analogous to natural products from secondary metabolites, such as flavonoids, is a promising source of novel drugs. Rutin (quercetin-3-O-rutinoside) is a natural flavone, which has, in its chemical structure, different sites for coordination with transition metals and the complexation with these metals enhances its biological properties. Rutin-zinc(II), a flavonoid-metal complex, was synthesized and characterized by UV-VIS, FT-IR, elemental analysis and H-1 NMR. The antioxidant and antitumor activities, as well as the cytotoxicity and in vivo toxicity of this complex were evaluated and compared with the free rutin. Rutin-zinc(II) has not shown any cytotoxicity against normal cells (fibroblasts and HUVECs) or toxicity in BALB/c mice, but has shown antioxidant activity in vitro and cytotoxicity against leukemia (KG1, K562 and Jurkat), multiple myeloma (RPMI8226) and melanoma (B16F10 and SK-Mel-28) cell lines in vitro. In Ehrlich ascites carcinoma model, Rutin-zinc(II) modulated the mitochondrial membrane potential and the expression of genes related to cell cycle progression, angiogenesis and apoptosis.
  • article 6 Citação(ões) na Scopus
    Differential expression of genes encoding proteins of the HGF/MET system in insulinomas
    (2015) MURAT, Cahue de Bernardis; ROSA, Paula Waki Lopes da; FORTES, Maria Angela Henriques Zanella; CORREA, Luciana; MACHADO, Marcel Cerqueira Cesar; NOVAK, Estela Maria; SIQUEIRA, Sheila Aparecida Coelho; PEREIRA, Maria Adelaide Albergaria; CORREA-GIANNELLA, Maria Lucia; GIANNELLA-NETO, Daniel; GIORGI, Ricardo Rodrigues
    Background: Insulinomas are the most common functional pancreatic neuroendocrine tumors, whereas histopathological features do not predict their biological behaviour. In an attempt to better understand the molecular processes involved in the tumorigenesis of islet beta cells, the present study evaluated the expression of genes belonging to the hepatocyte growth factor and its receptor (HGF/MET) system, namely, MET, HGF; HGFAC and ST14 (encode HGF activator and matriptase, respectively, two serine proteases that catalyze conversion of pro-HGF to active HGF); and SPINT1 and SPINT2 (encode serine peptidase inhibitors Kunitz type 1 and type 2, respectively, two inhibitors of HGF activator and of matriptase). Methods: Quantitative real-time reverse transcriptase polymerase chain reaction was employed to assess RNA expression of the target genes in 24 sporadic insulinomas: 15 grade 1 (G1), six grade 2 (G2) and three hepatic metastases. Somatic mutations of MET gene were searched by direct sequencing of exons 2, 10, 14, 16, 17 and 19. Results: Overexpression of MET was observed in the three hepatic metastases concomitantly with upregulation of the genes encoding HGF and matriptase and downregulation of SPINT1. A positive correlation was observed between MET RNA expression and Ki-67 proliferation index while a negative correlation was detected between SPINT1 expression and the mitotic index. No somatic mutations were found in MET gene. Conclusion: The final effect of the increased expression of HGF, its activator (matriptase) and its specific receptor (MET) together with a decreased expression of one potent inhibitor of matriptase (SPINT1) is probably a contribution to tumoral progression and metastatization in insulinomas.
  • conferenceObject
    BLM, FOXO3, FOXK2, FOXM1, FOXR1 genes as therapeutic targets to neuroblastoma
    (2018) GIMENEZ, Thamiris Magalhaes; NEVES, Nathalia Halley; SANTOS, Andreia Rangel; MARCHI, Fabio A.; KULIKOWSKI, Leslie; CRISTOFANI, Lilian M.; NOVAK, Estela M.; ODONE FILHO, Vicente
  • article 0 Citação(ões) na Scopus
    A model for preservation of thymocyte-depleted thymus
    (2023) DIAS, A. S.; DAMACENO-RODRIGUES, N. R.; GIMENEZ, T. M.; OLIVEIRA, P. M.; ZERBINI, M. C.; CARNEIRO-SAMPAIO, M.; FILHO, V. Odone; JATENE, M. B.; VASCONCELOS, D. M.; ROCHA, V.; NOVAK, E. M.
    DiGeorge syndrome is a disorder caused by a microdeletion on the long arm of chromosome 22. Approximately 1% of patients diagnosed with DiGeorge syndrome may have an absence of a functional thymus, which characterizes the complete form of the syndrome. These patients require urgent treatment to reconstitute T cell immunity. Thymus transplantation is a promising investigational procedure for reconstitution of thymic function in infants with congenital athymia. Here, we demonstrate a possible optimization of the preparation of thymus slices for transplantation through prior depletion of thymocytes and leukocyte cell lineages followed by cryopreservation with cryoprotective media (5% dextran FP 40, 5% Me2SO, and 5% FBS) while preserving tissue architecture. Thymus fragments were stored in liquid nitrogen at -196 & DEG;C for 30 days or one year. The tissue architecture of the fragments was preserved, including the distinction between medullary thymic epithelial cells (TECs), cortical TECs, and Hassall bodies. Moreover, depleted thymus fragments cryopreserved for one year were recolonized by intrathymic injections of 3 x 106 thymocytes per mL, demonstrating the capability of these fragments to support T cell development. Thus, this technique opens up the possibility of freezing and storing large volumes of thymus tissue for immediate transplantation into patients with DiGeorge syndrome or atypical (Omenn-like) phenotype.
  • bookPart
    Transcription Factors in Hematological Malignancies
    (2012) NOVAK, Estela Maria; MARIA, Durvanei Augusto
  • article 1 Citação(ões) na Scopus
    High-Resolution Magic-Angle-Spinning NMR in Revealing Hepatoblastoma Hallmarks
    (2022) TASIC, Ljubica; AVRAMOVIC, Natasa; JADRANIN, Milka; QUINTERO, Melissa; STANISIC, Danijela; MARTINS, Lucas G. G.; COSTA, Tassia Brena Barroso Carneiro; NOVAK, Estela; ODONE, Vicente; RIVAS, Maria; AGUIAR, Talita; CARRARO, Dirce Maria; CUNHA, Isabela Werneck da; COSTA, Cecilia Maria Lima da; MASCHIETTO, Mariana; KREPISCHI, Ana
    Cancer is one of the leading causes of death in children and adolescents worldwide; among the types of liver cancer, hepatoblastoma (HBL) is the most common in childhood. Although it affects only two to three individuals in a million, it is mostly asymptomatic at diagnosis, so by the time it is detected it has already advanced. There are specific recommendations regarding HBL treatment, and ongoing studies to stratify the risks of HBL, understand the pathology, and predict prognostics and survival rates. Although magnetic resonance imaging spectroscopy is frequently used in diagnostics of HBL, high-resolution magic-angle-spinning (HR-MAS) NMR spectroscopy of HBL tissues is scarce. Using this technique, we studied the alterations among tissue metabolites of ex vivo samples from (a) HBL and non-cancer liver tissues (NCL), (b) HBL and adjacent non-tumor samples, and (c) two regions of the same HBL samples, one more centralized and the other at the edge of the tumor. It was possible to identify metabolites in HBL, then metabolites from the HBL center and the border samples, and link them to altered metabolisms in tumor tissues, highlighting their potential as biochemical markers. Metabolites closely related to liver metabolisms such as some phospholipids, triacylglycerides, fatty acids, glucose, and amino acids showed differences between the tissues.
  • article 6 Citação(ões) na Scopus
    Gene expression profile suggesting immunological dysregulation in two Brazilian Bloom's syndrome cases
    (2020) MONTENEGRO, Marilia M.; QUAIO, Caio R.; PALMEIRA, Patricia; GASPARINI, Yanca; RANGEL-SANTOS, Andreia; DAMASCENO, Julian; NOVAK, Estela M.; GIMENEZ, Thamires M.; YAMAMOTO, Guilherme L.; RONJO, Rachel S.; NOVO-FILHO, Gil M.; CHEHIMI, Samar N.; ZANARDO, Evelin A.; DIAS, Alexandre T.; NASCIMENTO, Amom M.; COSTA, Thais V. M. M.; DUARTE, Alberto J. da S.; COUTINHO, Luiz L.; KIM, Chong A.; KULIKOWSKI, Leslie D.
    Background Bloom syndrome (BS) is a rare autosomal recessive chromosome instability disorder. The main clinical manifestations are growth deficiency, telangiectasic facial erythema, immunodeficiency, and increased risk to develop neoplasias at early age. Cytogenetic test for sister chromatid exchanges (SCEs) is used as a diagnostic marker for BS. In addition, most patients also present mutations in the & x202f;BLM & x202f;gene, related to defects in the DNA repair mechanism. However, the molecular mechanism behind the pathogenicity of BS is & x202f;still & x202f;not completely understood. Methods We describe two patients confirmed with BS by SCE and molecular analysis. Also, we performed the gene expression profile by the RNA-seq methodology in mRNA transcripts for differential gene expression analysis using as a biological condition for comparison BS versus health controls. Results We detected 216 differentially expressed genes related to immunological pathways such as positive regulation and activation of B cells, immune effector process and absence of difference of DNA repair genes expression. In addition; we also observed differentially expressed genes associated with apoptosis control, such as BCL2L1, CASP7, CDKN1A, E2F2, ITPR, CD274, TNFAIP6, TNFRSF25, TNFRSF13C, and TNFRSF17. Conclusion Our results suggest that the combination of altered expression of genes involved in signaling pathways of immune response and apoptosis control may contribute directly to the main characteristics observed in BS, such as recurrent infections, growth failure, and high risk of cancer. Transcriptome studies of other instability syndromes could allow a more accurate analysis of the relevant gene interactions associated with the destabilization of the genome. This is a first description of the profile of differential gene expression related to immunological aspects detected in patients with BS by RNA-seq.
  • conferenceObject
    MEG3 and MEG8 aberrant methylation associated with worst prognosis in an infant with neuroblastoma
    (2020) NOVAK, Estela M.; GIMENEZ, Thamiris Magalhaes; NEVES, Nathalia Halley; VINCE, Carolina Sgarioni Camargo; KREPISCHI, Ana Cristina Victorino; LAPA, Rainer Marco Lopez; CRISTOFANI, Lilian M.; BENDIT, Israel; ODONE FILHO, Vicente
  • article 5 Citação(ões) na Scopus
    Copy Number Alterations in Hepatoblastoma: Literature Review and a Brazilian Cohort Analysis Highlight New Biological Pathways
    (2021) BARROS, Juliana Sobral; AGUIAR, Talita Ferreira Marques; COSTA, Silvia Souza; RIVAS, Maria Prates; CYPRIANO, Monica; TOLEDO, Silvia Regina Caminada; NOVAK, Estela Maria; ODONE, Vicente; CRISTOFANI, Lilian Maria; CARRARO, Dirce Maria; CUNHA, Isabela Werneck da; COSTA, Cecilia Maria Lima; VIANNA-MORGANTE, Angela M.; ROSENBERG, Carla; KREPISCHI, Ana Cristina Victorino
    Hepatoblastoma (HB) is a rare embryonal tumor, although it is the most common pediatric liver cancer. The aim of this study was to provide an accurate cytogenomic profile of this type of cancer, for which information in cancer databases is lacking. We performed an extensive literature review of cytogenetic studies on HBs disclosing that the most frequent copy number alterations (CNAs) are gains of 1q, 2/2q, 8/8q, and 20; and losses at 1p and 4q. Furthermore, the CNA profile of a Brazilian cohort of 26 HBs was obtained by array-CGH; the most recurrent CNAs were the same as shown in the literature review. Importantly, HBs from female patients, high-risk stratification tumors, tumors who developed in older patients (> 3 years at diagnosis) or from patients with metastasis and/or deceased carried a higher diversity of chromosomal alterations, specifically chromosomal losses at 1p, 4, 11q and 18q. In addition, we distinguished three major CNA profiles: no detectable CNA, few CNAs and tumors with complex genomes. Tumors with simpler genomes exhibited a significant association with the epithelial fetal subtype of HBs; in contrast, the complex genome group included three cases with epithelial embryonal histology, as well as the only HB with HCC features. A significant association of complex HB genomes was observed with older patients who developed high-risk tumors, metastasis, and deceased. Moreover, two patients with HBs exhibiting complex genomes were born with congenital anomalies. Together, these findings suggest that a high load of CNAs, mainly chromosomal losses, particularly losses at 1p and 18, increases the tendency to HB aggressiveness. Additionally, we identified six hot-spot chromosome regions most frequently affected in the entire group: 1q31.3q42.3, 2q23.3q37.3, and 20p13p11.1 gains, besides a 5,3 Mb amplification at 2q24.2q24.3, and losses at 1p36.33p35.1, 4p14 and 4q21.22q25. An in-silico analysis using the genes mapped to these six regions revealed several enriched biological pathways such as ERK Signaling, MicroRNAs in Cancer, and the PI3K-Akt Signaling, in addition to the WNT Signaling pathway; further investigation is required to evaluate if disturbances of these pathways can contribute to HB tumorigenesis. The analyzed gene set was found to be associated with neoplasms, abnormalities of metabolism/homeostasis and liver morphology, as well as abnormal embryonic development and cytokine secretion. In conclusion, we have provided a comprehensive characterization of the spectrum of chromosomal alterations reported in HBs and identified specific genomic regions recurrently altered in a Brazilian HB group, pointing to new biological pathways, and relevant clinical associations.
  • bookPart
    Hematological Neoplasia and Angiogenesis: A Review
    (2012) NOVAK, Estela Maria