BRYAN ERIC STRAUSS

(Fonte: Lattes)
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Instituto do Câncer do Estado de São Paulo, Hospital das Clínicas, 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 - Líder

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Agora exibindo 1 - 9 de 9
  • conferenceObject
    Modifications of adenoviral structure and genome improves transduction efficiency and transgene expression
    (2015) VALLE, Paulo Roberto Del; ZANATTA, Daniela B.; STRAUSS, Bryan E.
  • conferenceObject
    PDIA1 overexpression activates acutely Nox1 NADPH oxidase in VSMC
    (2015) GONCALVES, Renata; ZANATA, Daniela; STRAUSS, Bryan; LAURINDO, Francisco Rafael; FERNANDES, Denise de Castro
  • conferenceObject
    Combined transfer of p19Arf and interferon-beta genes to mouse melanoma cells causes LC3B-and caspase-3-independent cell death and alters the expression of critical genes
    (2015) RIBEIRO, Aline H.; VALLE, Paulo R. Del; MEDRANO, Ruan F. V.; FERRARI, Daniel G.; ZANATTA, Daniela B.; STRAUSS, Bryan E.
  • bookPart
    Terapia gênica em câncer
    (2015) LANA, Marlous Vinícius Gomes; DAVID, Taynah Ibraim; STRAUSS, Bryan Eric
  • conferenceObject
    Silencing of apoptosome regulating genes, HSP70 and TRIAP1, induces apoptosis in MM cell lines
    (2015) ALYES, Veruska Lia Fook; ZANATTA, Daniela B.; OLIVEIRA, Mariana Bleker; EUGENIO, Angela Isabel Pereira; FERNANDO, Rodrigo Carlini; STRAUSS, Bryan E.; COLLEONI, Gisele Wally Braga
  • bookPart
    Ciclo celular e o reparo do DNS no câncer
    (2015) RIBEIRO, Aline Hunger; ZANATTA, Daniela Bertolini; STRAUSS, Bryan Eric
  • conferenceObject
  • article 16 Citação(ões) na Scopus
    Preservation of cardiac function in left ventricle cardiac hypertrophy using an AAV vector which provides VEGF-A expression in response to p53
    (2015) BAJGELMAN, Marcio C.; SANTOS, Leonardo dos; SILVA, Gustavo J. J.; NAKAMUTA, Juliana; SIRVENTE, Raquel A.; CHAVES, Marcio; KRIEGER, Jose Eduardo; STRAUSS, Bryan E.
    Here we present the application of our adeno-associated virus (AAV2) vector where transgene expression is driven by a synthetic, p53-responsive promoter, termed PG, used to supply human vascular endothelial growth factor-A(165) (VEGF-A). Thus, p53 is harnessed to promote the beneficial expression of VEGF-A encoded by the AAVPG vector, bypassing the negative effect of p53 on HIF-1 alpha which occurs during cardiac hypertrophy. Wistar rats were submitted to pressure overload induced by thoracic aorta coarctation (TAC) with or without concomitant gene therapy (intramuscular delivery in the left ventricle). After 12 weeks, rats receiving AAVPG-VEGF gene therapy were compared to those that did not, revealing significantly improved cardiac function under hemodynamic stress, lack of fibrosis and reversal of capillary rarefaction. With these functional assays, we have demonstrated that application of the AAVPG-VEGF vector under physiologic conditions known to stimulate p53 resulted in the preservation of cardiac performance.
  • article 22 Citação(ões) na Scopus
    Dermcidin exerts its oncogenic effects in breast cancer via modulation of ERBB signaling
    (2015) BANCOVIK, Jasna; MOREIRA, Dayson F.; CARRASCO, Daniel; YAO, Jun; PORTER, Dale; MOURA, Ricardo; CAMARGO, Anamaria; FONTES-OLIVEIRA, Cibely C.; MALPARTIDA, Miguel G.; CARAMBULA, Silvia; VANNIER, Edouard; STRAUSS, Bryan E.; WAKAMATSU, Alda; ALVES, Venancio A. F.; LOGULLO, Angela F.; SOARES, Fernando A.; POLYAK, Kornelia; BELIZARIO, Jose E.
    Background: We previously identified dermicidin (DCD), which encodes a growth and survival factor, as a gene amplified and overexpressed in a subset of breast tumors. Patients with DCD-positive breast cancer have worse prognostic features. We therefore searched for specific molecular signatures in DCD-positive breast carcinomas from patients and representative cell lines. Methods: DCD expression was evaluated by qRT-PCR, immunohistochemical and immunoblot assays in normal and neoplastic tissues and cell lines. To investigate the role of DCD in breast tumorigenesis, we analyzed the consequences of its downregulation in human breast cancer cell lines using three specific shRNA lentiviral vectors. Genes up- and down-regulated by DCD were identified using Affymetrix microarray and analyzed by MetaCore Platform. Results: We identified DCD splice variant (DCD-SV) that is co-expressed with DCD in primary invasive breast carcinomas and in other tissue types and cell lines. DCD expression in breast tumors from patients with clinical follow up data correlated with high histological grade, HER2 amplification and luminal subtype. We found that loss of DCD expression led to reduced cell proliferation, resistance to apoptosis, and suppressed tumorigenesis in immunodeficient mice. Network analysis of gene expression data revealed perturbed ERBB signaling following DCD shRNA expression including changes in the expression of ERBB receptors and their ligands. Conclusions: These findings imply that DCD promotes breast tumorigenesis via modulation of ERBB signaling pathways. As ERBB signaling is also important for neural survival, HER2+ breast tumors may highjack DCD's neural survival-promoting functions to promote tumorigenesis.