TATIANE KATSUE FURUYA

(Fonte: Lattes)
Índice h a partir de 2011
10
Lattes
ResearcherID
Projetos de Pesquisa
Unidades Organizacionais
Departamento de Radiologia, Faculdade de Medicina
LIM/05 - Laboratório de Poluição Atmosférica Experimental, Hospital das Clínicas, Faculdade de Medicina
LIM/24 - Laboratório de Oncologia Experimental, Hospital das Clínicas, Faculdade de Medicina

Filtros

Limpar filtros

Configurações

search.filters.applied.f.dateIssued: 2018 ×

Resultados de Busca

Agora exibindo 1 - 6 de 6
  • conferenceObject
    Correlation of a microRNA expression profile and the prognosis of penile cancer: A prospective study using microarray data analysis
    (2018) FURUYA, Tatiane K.; MURTA, Claudio B.; PONTES JR., Jose; UNO, Miyuki; CARRASCO, Alexis; SICHERO, Laura C.; VILLA, Luisa L.; COELHO, Rafael F.; GUGLIELMETTI, Giuliano B.; CORDEIRO, Mauricio D.; LEITE, Katia R.; SROUGI, Miguel; CHAMMAS, Roger; NAHAS, William C.
  • article 19 Citação(ões) na Scopus
    Association between Polymorphisms in Inflammatory Response-Related Genes and the Susceptibility, Progression and Prognosis of the Diffuse Histological Subtype of Gastric Cancer
    (2018) FURUYA, Tatiane K.; JACOB, Carlos E.; TOMITAO, Michele T. P.; CAMACHO, Lizeth C. C.; RAMOS, Marcus F. K. P.; ELUF-NETO, Jose; ALVES, Venancio A. F.; ZILBERSTEIN, Bruno; CECCONELLO, Ivan; RIBEIRO JR., Ulysses; CHAMMAS, Roger
    The chronic inflammatory microenvironment and immune cell dysfunction have been described as critical components for gastric tumor initiation and progression. The diffuse subtype is related to poor clinical outcomes, pronounced inflammation, and the worst prognosis. We investigated the association of polymorphisms in inflammatory response-related genes (COX-2, OGG1, TNFB, TNFA, HSPA1L, HSPA1B, VEGFA, IL17F, LGALS3, PHB, and TP53) with gastric cancer susceptibility, progression and prognosis in a Brazilian sample, focusing on the diffuse subtype. We also performed the analysis regarding the total sample of cases (not stratified for tumor subtypes), allowing the comparison between the findings. We further investigated the polymorphisms in linkage disequilibrium and performed haplotype association analyses. In the case-control study, rs1042522 (TP53) was associated with a stronger risk for developing gastric cancer in the sample stratified for diffuse subtype patients when compared to the risk observed for the total cases; CTC haplotype (rs699947 / rs833061 / rs2010963 VEGFA) was associated with risk while rs699947 was associated with protection for gastric malignancy in the total sample. Regarding the associations with the clinicopathological features of gastric cancer, for the diffuse subtype we found that rs699947 and rs833061 (VEGFA) were associated with outcomes related to a worse progression while rs5275 (COX-2), rs909253 (TNFB), and rs2227956 (HSPA1L) were associated to a better progression of the disease. In the total sample, rs699947 and rs833061 (VEGFA), rs4644 (LGALS3), and rs1042522 (TP53) were able to predict a worse progression while rs5275 (COX-2), rs2227956 (HSPA1L), and rs3025039 (VEGFA) a better progression. Besides, rs909253 (TNFB) predicted protection for the overall and disease-free survivals for gastric cancer. In conclusion, these results helped us to clarify the potential role of these polymorphisms in genes involved in the modulation of the inflammatory response in the pathogenesis of gastric cancer.
  • article 45 Citação(ões) na Scopus
    Pre- and postnatal exposure of mice to concentrated urban PM2.5 decreases the number of alveoli and leads to altered lung function at an early stage of life
    (2018) LOPES, Thais de Barros Mendes; GROTH, Espen E.; VERAS, Mariana; FURUYA, Tatiane K.; COSTA, Natalia de Souza Xavier; RIBEIRO JUNIOR, Gabriel; LOPES, Fernanda Degobbi; ALMEIDA, Francine M. de; CARDOSO, Wellington V.; SALDIVA, Paulo Hilario Nascimento; CHAMMAS, Roger; MAUAD, Thais
    Gestational exposure to air pollution is associated with negative outcomes in newborns and children. In a previous study, we demonstrated a synergistic negative effect of pre- and postnatal exposure to PM2.5 on lung development in mice. However, the means by which air pollution affects development of the lung have not yet been identified. In this study, we exposed pregnant BALB/c mice and their offspring to concentrated urban PM2.5 (from Sao Paulo, Brazil; target dose 600 mu g/m(3) for 1 h daily). Exposure was started on embryonic day 5.5 (E5.5, time of placental implantation). Lung tissue of fetuses and offspring was submitted to stereological and transcriptomic analyses at E14.5 (pseudoglandular stage of lung development), E18.5 (saccular stage) and P40 (postnatal day 40, alveolarized lung). Additionally, lung function and cellularity of bronchoalveolar lavage (BAL) fluid were studied in offspring animals at P40. Compared to control animals that were exposed to filtered air throughout gestation and postnatal life, PM-exposed mice exhibited higher lung elastance and a lower alveolar number at P40 whilst the total lung volume and cellularity of BAL fluid were not affected. Glandular and saccular structures of fetal lungs were not altered upon gestational exposure; transcriptomic signatures, however, showed changes related to DNA damage and its regulation, inflammation and regulation of cell proliferation. A differential expression was validated at E14.5 for the candidates Sox8, Angptl4 and Gas1. Our data substantiate the in utero biomolecular effect of gestational exposure to air pollution and provide first-time stereological evidence that pre- and early life-postnatal exposure compromise lung development, leading to a reduced number of alveoli and an impairment of lung function in the adult mouse.
  • conferenceObject
    Association between polymorphisms in inflammatory response related-genes and the susceptibility, progression, and prognosis of gastric cancer.
    (2018) FURUYA, Tatiane K.; JACOB, Carlos E.; TOMITAO, Michele T.; CORDOBA-CAMACHO, Lizeth C.; RAMOS, Marcus K.; ELUF-NETO, Jose; ALVES, Venancio A.; ZILBERSTEIN, Bruno; CECCONELLO, Ivan; RIBEIRO-JUNIOR, Ulysses; CHAMMAS, Roger
  • conferenceObject
    Correlation of microRNA expression profile and prognosis of penile cancer: A prospective study using microarray data analysis
    (2018) MURTA, Claudio Bovolenta; PONTES JR., Jose; FURUYA, Tatiane Katsue; UNO, Miyuki; CARRASCO, Alexis; SICHERO, Laura; VILLA, Luisa Lina; CORDEIRO, Mauricio; GUGLIELMETTI, Giuliano; COELHO, Rafael; LEITE, Katia Ramos Moreira; SROUGI, Miguel; CHAMMAS, Roger; NAHAS, William Carlos
  • article 30 Citação(ões) na Scopus
    Recurrent Copy Number Variants Associated with Syndromic Short Stature of Unknown Cause
    (2018) HOMMA, Thais K.; KREPISCHI, Ana C. V.; FURUYA, Tatiane K.; HONJO, Rachel S.; MALAQUIAS, Alexsandra C.; BERTOLA, Debora R.; COSTA, Silvia S.; CANTON, Ana P.; ROELA, Rosimeire A.; FREIRE, Bruna L.; KIM, Chong A.; ROSENBERG, Carla; JORGE, Alexander A. L.
    Background/Aims: Genetic imbalances are responsible for many cases of short stature of unknown etiology. This study aims to identify recurrent pathogenic copy number variants (CNVs) in patients with syndromic short stature of unknown cause. Methods: We selected 229 children with short stature and dysmorphic features, developmental delay, and/or intellectual disability, but without a recognized syndrome. All patients were evaluated by chromosomal microarray (array-based comparative genomic hybridization/single nucleotide polymorphism array). Additionally, we searched databases and previous studies to recover recurrent pathogenic CNVs associated with short stature. Results: We identified 32 pathogenic/probably pathogenic CNVs in 229 patients. By reviewing the literature, we selected 4 previous studies which evaluated CNVs in cohorts of patients with short stature. Taken together, there were 671 patients with short stature of unknown cause evaluated by chromosomal microarray. Pathogenic/probably pathogenic CNVs were identified in 87 patients (13%). Seven recurrent CNVs, 22q11.21, 15q26, 1p36.33, Xp22.33, 17p13.3, 1q21.1, 2q24.2, were observed. They are responsible for about 40% of all pathogenic/probably pathogenic genomic imbalances found in short stature patients of unknown cause. Conclusion: CNVs seem to play a significant role in patients with short stature. Chromosomal microarray should be used as a diagnostic tool for evaluation of growth disorders, especially for syndromic short stature of unknown cause. (C) 2017 S. Karger AG, Basel