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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Assunto: Oncology ×

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  • conferenceObject
    Anti-tumor Effect of P19Arf and Interferon-beta Gene Transference to Mouse Melanoma and Mouse Lung Carcinoma Cells is Revealed by a Strong Bystander Activity and a Potential Immune Response
    (2012) RIBEIRO, A. H.; MEDRANO, R. F. V.; CATANI, J. P. P.; STRAUSS, B. E.
    Introduction: Two hallmarks of tumor progression are resistance to cell death and lack of an effective anti-tumor immune response. Loss of p53 function, by genetic mutation or alterations in its pathway, such as p19Arf loss and/or mdm2 over-expression, inhibits one of the primary coordinators of cell death. Interferon-beta (IFN), a stimulator of the immune response with anti-neoplastic functions, is also frequently lost in some tumor types. We propose that p19Arf and IFN gene transfer would be an effective strategy, especially in wild-type p53 tumor cells, since cell death and immune activation would be combined to combat the tumor at primary treatment site and metastasis. Material and Methods: Recombinant adenoviral vectors with RGD-modified fiber (rAdRGD) and a p53-responsive promoter (PG) were constructed containing genes of p19Arf, IFN or the combination of both. Evaluation of in vitro antiproliferative effect of transgenes in B16F10 cells (B16, mouse melanoma, p53 wt) was done by annexin/PI staining and MTT assays. Bystander effect was revealed by cell cycle analysis of populations transduced with different proportions of the viruses. Antitumor effect in vivo was observed by treatment of established LLC1 tumors (mouse lung carcinoma, p53 wt) with intratumoral injection of rAdRGD in C57BL/6 mice. Involvement of immune response was revealed by second tumor challenge at contralateral flank of mice with a developed and treated first tumor. Results and Discussion: Cell death was resulted from the p19Arf and IFN combined transference (74% subG0), yet single gene transfer yielded only half the number of subG0 cells. A similar result was seen by measurement of cell viability with MTT. Evidence on a bystander effect was revealed when approximately 50% subG0 cells were observed, even though only 10% of the cells had been transduced with IFN. In a population of cells transduced with p19Arf, when 10% of them also expressed IFN, the number of subG0 cells increased to 68%, compared to transduction of p19Arf alone, which results in 45% subG0 cells. This indicates that p19Arf can sensitize cells to death by IFN bystander effect. In vivo assays with the LLC1 model have shown that in situ gene therapy of p19Arf and IFN combination was more effective to inhibit tumor progression and increase survival than application of a single gene. These animals were then challenged with the implantation of a second tumor, revealing greater retardation of growth at the secondary tumor site in mice treated with the combined gene therapy at the primary tumor locus as compared to animals that received single gene treatment. Conclusion: The use of p53-responsive vectors to express p19Arf and IFN represents a potential strategy for melanoma and lung carcinoma tumor suppression. We have shown that complementation of the p53/Arf and interferon pathways in the primary tumor may generate a strong bystander effect as well as immune stimulation.
  • 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.
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    Modifications of adenoviral structure and genome improves transduction efficiency and transgene expression
    (2015) VALLE, Paulo Roberto Del; ZANATTA, Daniela B.; STRAUSS, Bryan E.
  • article 13 Citação(ões) na Scopus
    Overhauling CAR T Cells to Improve Efficacy, Safety and Cost
    (2020) CHICAYBAM, Leonardo; BONAMINO, Martin H.; INVITTI, Adriana Luckow; ROZENCHAN, Patricia Bortman; VIEIRA, Igor de Luna; STRAUSS, Bryan E.
    Gene therapy is now surpassing 30 years of clinical experience and in that time a variety of approaches has been applied for the treatment of a wide range of pathologies. While the promise of gene therapy was over-stated in the 1990's, the following decades were met with polar extremes between demonstrable success and devastating setbacks. Currently, the field of gene therapy is enjoying the rewards of overcoming the hurdles that come with turning new ideas into safe and reliable treatments, including for cancer. Among these modalities, the modification of T cells with chimeric antigen receptors (CAR-T cells) has met with clear success and holds great promise for the future treatment of cancer. We detail a series of considerations for the improvement of the CAR-T cell approach, including the design of the CAR, routes of gene transfer, introduction of CARs in natural killer and other cell types, combining the CAR approach with checkpoint blockade or oncolytic viruses, improving pre-clinical models as well as means for reducing cost and, thus, making this technology more widely available. While CAR-T cells serve as a prime example of translating novel ideas into effective treatments, certainly the lessons learned will serve to accelerate the current and future development of gene therapy drugs.
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    A quantitative sequencing based method for the monitoring of clonal expansion
    (2012) STRAUSS, Bryan E.; ZANATTA, Daniela; AGUIAR, Rodrigo B. de
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    Use of p19Arf/interferon-beta immunotherapy in association with chemotherapy permits reduced drug dosage and avoids cardiotoxicity associated with doxorubicin
    (2019) STRAUSS, Bryan E.; MEDRANO, Ruan F. V.; TAMURA, Rodrigo; MENDONCA, Samir A.; FEITOSA, Valker A.; DARIOLLI, Rafael; SALLES, Thiago A.; HUNGER, Aline; CATANI, Joao P. P.; RODRIGUES, Elaine G.
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    Potentiation of doxorubicin low-dose efficacy through its association with p19Arf/Interferon-beta immunotherapy: Combining two immunogenic cell death inducers for the treatment of cancer.
    (2018) SR., Ruan F. V. Medrano; SR., Samir A. Mendonca; SR., Aline H. Ribeiro; SR., Joao P. P. Catani; SR., Valker A. Feitosa; SR., Elaine G. Rodrigues; SR., Bryan E. Strauss
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  • article 21 Citação(ões) na Scopus
    Combined p19Arf and interferon-beta gene transfer enhances cell death of B16 melanoma in vitro and in vivo
    (2013) MERKEL, C. A.; MEDRANO, R. F. V.; BARAUNA, V. G.; STRAUSS, B. E.
    Approximately 90% of melanomas retain wild-type p53, a characteristic that may help shape the development of novel treatment strategies. Here, we employed an adenoviral vector where transgene expression is,controlled by p53 to deliver the p19 alternate reading frame (An) and interferon-beta (IFN beta) complementary DNAs in the B16 mouse model of melanoma. In vitro, cell death was enhanced by combined gene transfer (63.82 +/- 15.30% sub-GO cells); yet introduction of a single gene resulted in significantly fewer hypoploid cells (37.73 +/- 7.3% or 36.96 +/- 11.58%, p19Arf or IFN beta, respectively, P < 0.05). Annexin V staining and caspase-3 cleavage indicate a cell death mechanism consistent with apoptosis. Using reverse transcriptase quantitative PCR, we show that key transcriptional targets of p53 were upregulated in the presence of p19Arf, although treatment with IFN beta did not alter expression of the genes studied. In situ gene therapy revealed significant inhibition of subcutaneous tumors by IFN beta (571 +/- 25 mm(3)) or the combination of p19Arf and IFN beta (489 +/- 124 mm(3)) as compared with the LacZ control (1875 +/- 33 mm(3), P < 0.001); whereas p19Arf yielded an intermediate result (1053 +/- 169 mm(3), P < 0.01 vs control). However, only the combination was associated with increased cell death and prolonged survival (P < 0.01). As shown here, the combined transfer of p19Arf and IFN beta using p53-responsive vectors enhanced cell death both in vitro and in vivo.