EMERSON SOARES BERNARDES

EMERSON SOARES BERNARDES

(Fonte: Lattes)

Resumo

Bachelor's at Farmácia from Universidade Federal de Ouro Preto (1998) and doctorate at Applied Imunology from Universidade de São Paulo (2004). Has experience in Medicine, acting on the following subjects: galectina-3, carboidratos, trypanosoma cruzi, carcinogênesis and macrophage. (Text obtained from the Currículo Lattes on October 8th 2021)

Possui graduação em Farmácia pela Universidade Federal de Ouro Preto (1998), mestrado e doutorado em Imunologia Básica e Aplicada pela Faculdade de Medicina de Ribeirão Preto, Universidade de São Paulo (2004), com período de Doutorado Sanduíche pela Universidade da California, Davis, USA. Realizou pós-doutoramento durante o período de 2004 a 2008 pela Faculdade de Medicina da USP-Ribeirão Preto. Trabalhou como pesquisador contratado pelo Instituto de Patologia e Imunologia Molecular da Universidade do Porto - IPATIMUP em Portugal no período de 2008 a 2011. Retornou ao Brasil como pesquisador visitante na Faculdade de Medicina da USP - São Paulo (2011-2012) e foi posteriormente contratado como pesquisador no Instituto do Câncer do Estado de São Paulo (2012-2013). Coordenou um projeto Jovem Pesquisador financiado pela FAPESP (2012-2016 - Desenvolvimento e Produção de Radiofármacos Emissores de Pósitrons com Aplicações Diagnósticas em Oncologia) e está integrado como pesquisador Colaborador no Instituto de Pesquisas Energéticas e Nucleares (IPEN). Tem atuado na área da Glicobiologia, com ênfase na participação de proteínas ligantes de carboidratos em processos inflamatórios e no Câncer. Atualmente é professor do Programa de Pós-Graduação do IPEN-USP Tecnologia Nuclear - Aplicações, tem experiência na área de Radiofarmácia, com ênfase no desenvolvimento de Radiofármacos inéditos para diagnóstico e terapia em Oncologia. (Texto extraído do Currículo Lattes em 08 out. 2021)

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Recognition of breast cancer subtypes using FTIR hyperspectral data
2024 - FAROOQ, SAJID; DEL-VALLE, MATHEUS; SANTOS, SOFIA N. dos; BERNARDES, EMERSON S.; ZEZELL, DENISE M.
Fourier -transform infrared spectroscopy (FTIR) is a powerful, non-destructive, highly sensitive and a promising analytical technique to provide spectrochemical signatures of biological samples, where markers like carbohydrates, proteins, and phosphate groups of DNA can be recognized in biological micro -environment. However, method of measurements of large cells need an excessive time to achieve high quality images, making its clinical use difficult due to speed of data -acquisition and lack of optimized computational procedures. To address such challenges, Machine Learning (ML) based technologies can assist to assess an accurate prognostication of breast cancer (BC) subtypes with high performance. Here, we applied FTIR spectroscopy to identify breast cancer subtypes in order to differentiate between luminal (BT474) and nonluminal (SKBR3) molecular subtypes. For this reason, we tested multivariate classification technique to extract feature information employing three -dimension (3D) -discriminant analysis approach based on 3D -principle component analysis -linear discriminant analysis (3D-PCA-LDA) and 3D -principal component analysis -quadratic discriminant analysis (3D-PCA-QDA), showing an improvement in sensitivity (98%), specificity (94%) and accuracy (98%) parameters compared to conventional unfolded methods. Our results evidence that 3D-PCALDA and 3D-PCA-QDA are potential tools for discriminant analysis of hyperspectral dataset to obtain superior classification assessment.
Plant-derived polyphenolic compounds
2023 - ROSALES, THIECLA K.O.; SILVA, FABIO F.A. da; BERNARDES, EMERSON S.; FABI, JOAO P.
Plant-derived polyphenols are naturally occurring compounds widely distributed in plants. They have received greater attention in the food and pharmaceutical industries due to their potential health benefits, reducing the risk of some chronic diseases due to their antioxidant, anti-inflammatory, anticancer, cardioprotective, and neuro-action properties. Polyphenolic compounds orally administered can be used as adjuvants in several treatments but with restricted uses due to chemical instability. The review discusses the different structural compositions of polyphenols and their influence on chemical stability. Despite the potential and wide applications, there is a need to improve the delivery of polyphenolics to target the human intestine without massive chemical modifications. Oral administration of polyphenols is unfeasible due to instability, low bioaccessibility, and limited bioavailability. Nano-delivery systems based on polysaccharides (starch, pectin, chitosan, and cellulose) have been identified as a viable option for oral ingestion, potentiate biological effects, and direct-controlled delivery in specific tissues. The time and dose can be individualized for specific diseases, such as intestinal cancer. This review will address the mechanisms by which polysaccharides-based nanostructured systems can protect against degradation and enhance intestinal permeation, oral bioavailability, and the potential application of polysaccharides as nanocarriers for the controlled and targeted delivery of polyphenolic compounds.
Synthesis, biological evaluation and molecular docking studies of novel 1,2,3-triazole-quinazolines as antiproliferative agents displaying ERK inhibitory activity
2021 - NUNES, PAULO S.G.; SILVA, GABRIEL da; NASCIMENTO, SOFIA; MANTOANI, SUSIMAIRE P.; ANDRADE, PETERSON de; BERNARDES, EMERSON S.; KAWANO, DANIEL F.; LEOPOLDINO, ANDREIA M.; CARVALHO, IVONE
ERK1/2 inhibitors have attracted special attention concerning the ability of circumventing cases of innate or log-term acquired resistance to RAF and MEK kinase inhibitors. Based on the 4-aminoquinazoline pharmacophore of kinases, herein we describe the synthesis of 4-aminoquinazoline derivatives bearing a 1,2,3-triazole stable core to bridge different aromatic and heterocyclic rings using copper-catalysed azide-alkyne cycloaddition reaction (CuAAC) as a Click Chemistry strategy. The initial screening of twelve derivatives in tumoral cells (CAL-27, HN13, HGC-27, and BT-20) revealed that the most active in BT-20 cells (25a, IC50 24.6 μM and a SI of 3.25) contains a more polar side chain (sulfone). Furthermore, compound 25a promoted a significant release of lactate dehydrogenase (LDH), suggesting the induction of cell death by necrosis. In addition, this compound induced G0/G1 stalling in BT-20 cells, which was accompanied by a decrease in the S phase. Western blot analysis of the levels of p-STAT3, p-ERK, PARP, p53 and cleaved caspase-3 revealed p-ERK1/2 and p-STA3 were drastically decreased in BT-20 cells under 25a incubation, suggesting the involvement of these two kinases in the mechanisms underlying 25a-induced cell cycle arrest, besides loss of proliferation and viability of the breast cancer cell. Molecular docking simulations using the ERK-ulixertinib crystallographic complex showed compound 25a could potentially compete with ATP for binding to ERK in a slightly higher affinity than the reference ERK1/2 inhibitor. Further in silico analyses showed comparable toxicity and pharmacokinetic profiles for compound 25a in relation to ulixertinib.
O-glycan sialylation alters galectin-3 subcellular localization and decreases chemotherapy sensitivity in gastric cancer
2016 - SANTOS, SOFIA N.; JUNQUEIRA, MARA S.; FRANCISCO, GUILHERME; VILANOVA, MANUEL; MAGALHAES, ANA; BARUFFI, MARCELO D.; CHAMMAS, ROGER; HARRIS, ADRIAN L.; REIS, CELSO A.; BERNARDES, EMERSON S.
ST6GalNAc-I, the sialyltransferase responsible for sialyl-Tn (sTn) synthesis, has been previously reported to be positively associated with cancer aggressiveness. Here we describe a novel sTn-dependent mechanism for chemotherapeutic resistance. We show that sTn protects cancer cells against chemotherapeutic-induced cell death by decreasing the interaction of cell surface glycan receptors with galectin-3 and increasing its intracellular accumulation. Moreover, exogenously added galectin-3 potentiated the chemotherapeutics-induced cytotoxicity in sTn non-expressing cells, while sTn overexpressing cells were protected. We also found that the expression of sTn was associated with a reduction in galectin-3-binding sites in human gastric samples tumors. ST6GalNAc-I knockdown restored galectin-3-binding sites on the cell surface and chemotherapeutics sensibility. Our results clearly demonstrate that an interruption of O-glycans extension caused by ST6GalNAc-I enzymatic activity leads to tumor cells resistance to chemotherapeutic drugs, highlighting the need for the development of novel strategies to target galectin-3 and/or ST6GalNAc-I.