| Grant number: | 11/10656-5 |
| Support Opportunities: | Scholarships in Brazil - Doctorate |
| Start date: | December 01, 2011 |
| End date: | November 30, 2015 |
| Field of knowledge: | Biological Sciences - Biochemistry - Molecular Biology |
| Principal Investigator: | Bryan Eric Strauss |
| Grantee: | Aline Hunger Ribeiro |
| Host Institution: | Instituto do Câncer do Estado de São Paulo Octavio Frias de Oliveira (ICESP). Coordenadoria de Serviços de Saúde (CSS). Secretaria da Saúde (São Paulo - Estado). São Paulo , SP, Brazil |
Abstract Malignant melanoma is type of cancer with high death rates due, in part, to its propensity to form metastases. Approximately 90% of melanoma cases maintain wild-type p53 and perhaps this could be used as a tool to drive expression from the vector interest. Viral Vector Group (VVG - Incor - FMUSP) has developed adenoviral vectors in which transgene expression is controlled by the transcription factor and tumor suppressor, p53. The VVG has also improved these vectors by modifying the fiber knob protein, allowing efficient transduction of a wide range of target cells without dependence on the wild-type adenovirus receptor, CAR. Using these vectors, the VVG has shown that combined treatment with p19Arf and IFN-beta together, but not alone, had induced B16 (murine melanoma) cell death. In this regard, we propose new studies to identify critical genes activated by the combined treatment and that act as mediators in the cellular response to the gene transfer strategy. In this project, we will transfer the combination of the p19Arf and IFN-beta to B16 cells and compare gene expression profile of these cells and cells that have received only one of these factors. We will also perform functional assays in order to verify the role of the factors identified upon treatment with the viral vectors. In addition, subcellular localization, post-translational modifications and protein interactions known to be critical for p53/ARF or IFN-beta will be evaluated after viral treatment. We hope that elucidation of molecular mechanisms involved in the response of melanoma cells to the combined p19Arf and IFN-beta treatments could be useful for understanding tumor biology and, possibly, shape new therapeutic interventions. | |
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