| Grant number: | 11/10459-5 |
| Support Opportunities: | Regular Research Grants |
| Start date: | September 01, 2011 |
| End date: | August 31, 2013 |
| Field of knowledge: | Health Sciences - Medicine - Medical Clinics |
| Principal Investigator: | Silvia Regina Caminada de Toledo |
| Grantee: | Silvia Regina Caminada de Toledo |
| Host Institution: | Escola Paulista de Medicina (EPM). Universidade Federal de São Paulo (UNIFESP). Campus São Paulo. São Paulo , SP, Brazil |
| Associated researchers: | Antonio Sergio Petrilli ; Carla Renata Pacheco Donato Macedo ; Indhira Dias Oliveira ; Maria Teresa de Seixas Alves ; Simone de Campos Vieira Abib |
Abstract
Sarcomas are a heterogeneous group of malignant tumors with a high frequency in children. From a genetic standpoint, sarcomas can be divided into two main groups, which are distinguishable by cytogenetic findings. One group is characterized by the presence of simple karyotypes, near diploid, with a few specific chromosomal changes, which include the rhabdomyosarcoma (RMS), Ewing's sarcoma (ES) and synovial sarcoma (SS). The second group presents complex karyotypes with a high degree of genomic instability, in which it characterizes osteosarcoma (OS). Although chemotherapeutic agents and surgical techniques vary with the type of cancer and location of disease, sarcomas, bone and soft tissue share a common characteristic: the survival curves for these diseases remain stagnant in the last two decades, despite the numerous clinical protocols and various agents used. The objective of this study will be the evaluation of the expression profile of fusion and development genes in RMS, SE and SS, and the role of MAPK7 gene in OS. RT-PCR, qPCR will be performed to analyze the fusion genes: PAX3-FKHR, PAX7-FKHR, EWS-FLI1, SYT-SSX1, SYT-SSX2 and development genes: IGF2, IHH, GLI1 and PTCH1 in RMS, SE and SS tumors. In OS evaluate if the increased expression of the MAPK7 gene, observed in a previous study, is results from a mutation of this gene by sequencing. It will be performed MAPK7 gene silencing and later we will carry out technical viability, proliferation, apoptosis, migration and invasion in silenced and not silenced OS cells, so that we can elucidate the role of MAPK7 gene as a possible prognostic marker in OS. (AU)
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