BRYAN ERIC STRAUSS

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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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Colaboração internacional: Estados Unidos ×

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Agora exibindo 1 - 8 de 8
  • article 635 Citação(ões) na Scopus
    Consensus guidelines for the definition, detection and interpretation of immunogenic cell death
    (2020) GALLUZZI, Lorenzo; VITALE, Ilio; WARREN, Sarah; ADJEMIAN, Sandy; AGOSTINIS, Patrizia; MARTINEZ, Aitziber Buque; CHAN, Timothy A.; COUKOS, George; DEMARIA, Sandra; DEUTSCH, Eric; DRAGANOV, Dobrin; EDELSON, Richard L.; FORMENTI, Silvia C.; FUCIKOVA, Jitka; GABRIELE, Lucia; GAIPL, Udo S.; GAMEIRO, Sofia R.; GARG, Abhishek D.; GOLDEN, Encouse; HAN, Jian; HARRINGTON, Kevin J.; HEMMINKI, Akseli; HODGE, James W.; HOSSAIN, Dewan Md Sakib; ILLIDGE, Tim; KARIN, Michael; KAUFMAN, Howard L.; KEPP, Oliver; KROEMER, Guido; LASARTE, Juan Jose; LOI, Sherene; LOTZE, Michael T.; MANIC, Gwenola; MERGHOUB, Taha; MELCHER, Alan A.; MOSSMAN, Karen L.; PROSPER, Felipe; REKDAL, Oystein; RESCIGNO, Maria; RIGANTI, Chiara; SISTIGU, Antonella; SMYTH, Mark J.; SPISEK, Radek; STAGG, John; STRAUSS, Bryan E.; TANG, Daolin; TATSUNO, Kazuki; GOOL, Stefaan W. van; VANDENABEELE, Peter; YAMAZAKI, Takahiro; ZAMARIN, Dmitriy; ZITVOGEL, Laurence; CESANO, Alessandra; MARINCOLA, Francesco M.
    Cells succumbing to stress via regulated cell death (RCD) can initiate an adaptive immune response associated with immunological memory, provided they display sufficient antigenicity and adjuvanticity. Moreover, multiple intracellular and microenvironmental features determine the propensity of RCD to drive adaptive immunity. Here, we provide an updated operational definition of immunogenic cell death (ICD), discuss the key factors that dictate the ability of dying cells to drive an adaptive immune response, summarize experimental assays that are currently available for the assessment of ICD in vitro and in vivo, and formulate guidelines for their interpretation.
  • article 0 Citação(ões) na Scopus
    Interferons: key modulators of the immune system in cancer
    (2023) YUSUF, Nabiha; ALLIE, S. Rameeza; STRAUSS, Bryan E.
  • article 2 Citação(ões) na Scopus
    Potentiation of combined p19Arf and interferon-beta cancer gene therapy through its association with doxorubicin chemotherapy
    (2022) V, Ruan F. Medrano; SALLES, Thiago A.; DARIOLLI, Rafael; ANTUNES, Fernanda; FEITOSA, Valker A.; HUNGER, Aline; CATANI, Joao P. P.; MENDONCA, Samir A.; TAMURA, Rodrigo E.; LANA, Marlous G.; RODRIGUES, Elaine G.; STRAUSS, Bryan E.
    Balancing safety and efficacy is a major consideration for cancer treatments, especially when combining cancer immunotherapy with other treatment modalities such as chemotherapy. Approaches that induce immunogenic cell death (ICD) are expected to eliminate cancer cells by direct cell killing as well as activation of an antitumor immune response. We have developed a gene therapy approach based on p19Arf and interferon-beta gene transfer that, similar to conventional inducers of ICD, results in the release of DAMPS and immune activation. Here, aiming to potentiate this response, we explore whether association between our approach and treatment with doxorubicin (Dox), a known inducer of ICD, could further potentiate treatment efficacy without inducing cardiotoxicity, a critical side effect of Dox. Using central composite rotational design analysis, we show that cooperation between gene transfer and chemotherapy killed MCA205 and B16F10 cells and permitted the application of reduced viral and drug doses. The treatments also cooperated to induce elevated levels of ICD markers in MCA205, which correlated with improved efficacy of immunotherapy in vivo. Treatment of subcutaneous MCA205 tumors associating gene transfer and low dose (10 mg/kg) chemotherapy resulted in inhibition of tumor progression. Moreover, the reduced dose did not cause cardiotoxicity as compared to the therapeutic dose of Dox (20 mg/kg). The association of p19Arf/interferon-beta gene transfer and Dox chemotherapy potentiated antitumor response and minimized cardiotoxicity.
  • article 20 Citação(ões) na Scopus
    Targeting MAGE-C1/CT7 Expression Increases Cell Sensitivity to the Proteasome Inhibitor Bortezomib in Multiple Myeloma Cell Lines
    (2011) CARVALHO, Fabricio de; COSTA, Erico T.; CAMARGO, Anamaria A.; GREGORIO, Juliana C.; MASOTTI, Cibele; ANDRADE, Valeria C. C.; STRAUSS, Bryan E.; CABALLERO, Otavia L.; ATANACKOVIC, Djordje; COLLEONI, Gisele W. B.
    The MAGE-C1/CT7 encodes a cancer/testis antigen (CTA), is located on the chromosomal region Xq26-27 and is highly polymorphic in humans. MAGE-C1/CT7 is frequently expressed in multiple myeloma (MM) that may be a potential target for immunotherapy in this still incurable disease. MAGEC1/CT7 expression is restricted to malignant plasma cells and it has been suggested that MAGE-C1/CT7 might play a pathogenic role in MM; however, the exact function this protein in the pathophysiology of MM is not yet understood. Our objectives were (1) to clarify the role of MAGE-C1/CT7 in the control of cellular proliferation and cell cycle in myeloma and (2) to evaluate the impact of silencing MAGE-C1/CT7 on myeloma cells treated with bortezomib. Myeloma cell line SKO-007 was transduced for stable expression of shRNA-MAGE-C1/CT7. Downregulation of MAGE-C1/CT7 was confirmed by real time quantitative PCR and western blot. Functional assays included cell proliferation, cell invasion, cell cycle analysis and apoptosis. Western blot showed a 70-80% decrease in MAGE-C1/CT7 protein expression in inhibited cells (shRNA-MAGE-C1/CT7) when compared with controls. Functional assays did not indicate a difference in cell proliferation and DNA synthesis when inhibited cells were compared with controls. However, we found a decreased percentage of cells in the G2/M phase of the cell cycle among inhibited cells, but not in the controls (p < 0.05). When myeloma cells were treated with bortezomib, we observed a 48% reduction of cells in the G2/M phase among inhibited cells while controls showed 13% (empty vector) and 9% (ineffective shRNA) reduction, respectively (p < 0.01). Furthermore, inhibited cells treated with bortezomib showed an increased percentage of apoptotic cells (Annexin V+/PI-) in comparison with bortezomib-treated controls (p < 0.001). We found that MAGE-C1/CT7 protects SKO-007 cells against bortezomib-induced apoptosis. Therefore, we could speculate that MAGE-C1/CT7 gene therapy could be a strategy for future therapies in MM, in particular in combination with proteasome inhibitors.
  • article 3 Citação(ões) na Scopus
    Exploration of p53 plus interferon-beta gene transfer for the sensitization of human colorectal cancer cell lines to cell death
    (2021) VALLE, Paulo Roberto Del; MENDONCA, Samir Andrade; ANTUNES, Fernanda; HUNGER, Aline; TAMURA, Rodrigo E.; ZANATTA, Daniela Bertolini; STRAUSS, Bryan E.
    While treatments for colorectal cancer continue to improve, some 50% of patients succumb within 5 years, pointing to the need for additional therapeutic options. We have developed a modified non-replicating adenoviral vector for gene transfer, called AdRGD-PG, which offers improved levels of transduction and transgene expression. Here, we employ the p53-responsive PG promoter to drive expression of p53 or human interferon-beta (hIFN beta) in human colorectal cancer cell lines HCT116(wt) (wtp53), HCT116(-/-) (p53 deficient) and HT29 (mutant p53). The HCT116 cell lines were both easily killed with p53 gene transfer, while combined p53 and hIFN beta cooperated for the induction of HT29 cell death and emission of immunogenic cell death (ICD) markers. Elevated annexinV staining and caspase 3/7 activity point to cell death by a mechanism consistent with apoptosis. P53 gene transfer alone or in combination with hIFN beta sensitized all cell lines to chemotherapy, permitting the application of low drug doses while still achieving significant loss of viability. While endogenous p53 status was not sufficient to predict response to treatment, combined p53 and hIFN beta provided an additive effect in HT29 cells. We propose that this approach may prove effective for the treatment of colorectal cancer, permitting the use of limited drug doses.
  • article 1 Citação(ões) na Scopus
    Induction of Immune-Stimulating Factors and Oncolysis Upon p14(ARF) Gene Transfer in Melanoma Cell Lines
    (2023) MENDONCA, Samir Andrade; ANTUNES, Fernanda; CERQUEIRA, Otto L. D.; VALLE, Paulo Roberto Del; HUNGER, Aline; OLIVEIRA, Percillia V. S. de; BRITO, Barbara; COSTANZI-STRAUSS, Eugenia; STRAUSS, Bryan E.
    Together with an anti-tumor immune response, oncolysis using a recombinant viral vector promises to eliminate cancer cells by both gene transfer and host-mediated functions. In this study we explore oncolysis induced by nonreplicating adenoviral vectors used for p14(ARF) and interferon-beta (hIFN beta) gene transfer in human melanoma cell lines, revealing an unexpected role for p14(ARF) in promoting cellular responses predictive of immune stimulation. Oncolysis was confirmed when UACC-62 (p53 wild-type) cells succumbed upon p14(ARF) gene transfer in vitro, whereas SK-Mel-29 (p53-mutant) benefitted from its combination with hIFN beta. In the case of UACC-62, in situ gene therapy in nude mice yielded reduced tumor progression in response to the p14(ARF) and hIFN beta combination. Potential for immune stimulation was revealed where p14(ARF) gene transfer in vitro was sufficient to induce emission of immunogenic cell death factors in UACC-62 and upregulate pro-immune genes, including IRF1, IRF7, IRF9, ISG15, TAP-1, and B2M. In SK-Mel-29, p14(ARF) gene transfer induced a subset of these factors. hIFN beta was, as expected, sufficient to induce these immune-stimulating genes in both cell lines. This work is a significant advancement for our melanoma gene therapy strategy because we revealed not only the induction of oncolysis, but also the potential contribution of p14(ARF) to immune stimulation.
  • article 7 Citação(ões) na Scopus
    Metformin-induced chemosensitization to cisplatin depends on P53 status and is inhibited by Jarid1b overexpression in non-small cell lung cancer cells
    (2021) TORTELLI JR., Tharcisio Citrangulo; TAMURA, Rodrigo Esaki; JUNQUEIRA, Mara de Souza; MORORO, Janio da Silva; BUSTOS, Silvina Odete; NATALINO, Renato Jose Mendonca; RUSSELL, Shonagh; DESAUBRY, Laurent; STRAUSS, Bryan Eric; CHAMMAS, Roger
    Metformin has been tested as an anti-cancer therapy with potential to improve conventional chemotherapy. However, in some cases, metformin fails to sensitize tumors to chemotherapy. Here we test if the presence of P53 could predict the activity of metformin as an adjuvant for cisplatin-based therapy in non-small cell lung cancer (NSCLC). A549, HCC 827 (TP53 WT), H1299, and H358 (TP53 null) cell lines were used in this study. A549 cells were pre-treated with a sub-lethal dose of cisplatin to induce chemoresistance. The effects of metformin were tested both in vitro and in vivo and related to the ability of cells to accumulate Jarid1b, a histone demethylase involved in cisplatin resistance in different cancers. Metformin sensitized A549 and HCC 827 cells (but not H1299 and H358 cells) to cisplatin in a P53-dependent manner, changing its subcellular localization to the mitochondria. Treatment with a sub-lethal dose of cisplatin increased Jarid1b expression, yet downregulated P53 levels, protecting A549Res cells from metformin-induced chemosensitization to cisplatin and favored a glycolytic phenotype. Treatment with FL3, a synthetic flavagline, sensitized A549Res cells to cisplatin. In conclusion, metformin could potentially be used as an adjuvant for cisplatin-based therapy in NSCLC cells if wild type P53 is present.
  • article 21 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.