Between 2010 and 2014, he served as Vice-Coordinator of the Bachelor's Degree in Biotechnology and later was Head of the Department of Genetics and Evolution from 2014 to 2017. He is currently the Coordinator of the Graduate Program in Biotechnology at UFSCar. He is a Level 2 Researcher at CNPq, and his main research interests include: gene expression related to erythrocyte diseases in humans; the identification of thermotolerant and ethanol-resistant yeasts for application in alcoholic fermentation; and the isolation and adaptation of yeasts for the production of fermented beverages such as beer and wine. Additionally, he has dedicated himself to studies of genomic and transcriptomic analyses in termites, focusing on control targets, genes related to development, and the search for proteins of biotechnological interest. Recently, he has been conducting research in the area of soil microbiome, aiming to identify microorganisms that can be used as markers of soil health, as well as elem
EDUCATION
Bachelor's degree in Biological Sciences from the State University of Campinas (1997) and a PhD in Functional and Molecular Biology from the same institution (2004). Currently, he is an Associate Professor at the Federal University of São Carlos (UFSCar), where he coordinates the Laboratory of Biochemistry and Applied Genetics, working in the Department of Genetics and Evolution
RESEARCH, TEACHING, or OTHER INTERESTS
Biochemistry, Genetics and Molecular Biology, Molecular Biology, Genetics, Biotechnology
Identification of target genes using gene expression profile of granulocytes from patients with chronic myeloid leukemia treated with tyrosine kinase inhibitors Cintia do Couto Mascarenhas, Anderson Ferreira da Cunha, Ana Flávia Brugnerotto, Sheley Gambero, Maria Helena de Almeida, et al. Leukemia and Lymphoma, 2014 Differential gene expression analysis by suppression subtractive hybridization with correlation to the metabolic pathways involved in chronic myeloid leukemia (CML) may provide a new insight into the pathogenesis of CML. Among the overexpressed genes found in CML at diagnosis are SEPT5, RUNX1, MIER1, KPNA6 and FLT3, while PAN3, TOB1 and ITCH were decreased when compared to healthy volunteers. Some genes were identified and involved in CML for the first time, including TOB1, which showed a low expression in patients with CML during tyrosine kinase inhibitor treatment with no complete cytogenetic response. In agreement, reduced expression of TOB1 was also observed in resistant patients with CML compared to responsive patients. This might be related to the deregulation of apoptosis and the signaling pathway leading to resistance. Most of the identified genes were related to the regulation of nuclear factor κB (NF-κB), AKT, interferon and interleukin-4 (IL-4) in healthy cells. The results of this study combined with literature data show specific gene pathways that might be explored as markers to assess the evolution and prognosis of CML as well as identify new therapeutic targets.
Gene expression profiles of erythroid precursors characterise several mechanisms of the action of hydroxycarbamide in sickle cell anaemia Flávia Chagas Costa, Anderson Ferreira da Cunha, André Fattori, Tarcísio De Sousa Peres, Gustavo Gilson Lacerda Costa, et al. British Journal of Haematology, 2007 SummaryHydroxycarbamide (HC) (or hydroxyurea) has been reported to increase fetal haemoglobin levels and improve clinical symptoms in sickle cell anaemia (SCA) patients. However, the complete pathway by which HC acts remains unclear. To study the mechanisms involved in the action of HC, global gene expression profiles were obtained from the bone marrow cells of a SCA patient before and after HC treatment using serial analysis of gene expression. In the comparison of both profiles, 147 differentially expressed transcripts were identified. The functional classification of these transcripts revealed a group of gene categories associated with transcriptional and translational regulation, e.g. EGR‐1, CENTB1, ARHGAP4 and RIN3, suggesting a possible role for these pathways in the improvement of clinical symptoms of SCA patients. The genes involved in these mechanisms may represent potential tools for the identification of new targets for SCA therapy.
