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Comparative study of immunotherapy treatments for chemically induced rat ovarian cancer

Grant number: 19/18053-0
Support type:Scholarships in Brazil - Post-Doctorate
Effective date (Start): January 01, 2021
Effective date (End): December 31, 2022
Field of knowledge:Biological Sciences - Immunology - Applied Immunology
Principal researcher:Wagner José Fávaro
Grantee:Gabriela de Oliveira
Home Institution: Instituto de Biologia (IB). Universidade Estadual de Campinas (UNICAMP). Campinas , SP, Brazil

Abstract

In Brazil ovarian cancer is the seventh most common cancer in the Midwest, Northeast and North regions, and the eighth most common in women in the South and Southeast regions. In Brazil, approximately 6150 new cases are estimated between 2018 and 2019, with an estimated risk of 5.79 cases per 100,000 women. The average age of women with these tumors is 60 years, and the risk of developing ovarian cancer throughout life is 1 in 70. The symptoms of ovarian cancer are not specific. The treatment in turn has been six cycles of carboplatin and paclitaxel, this treatment has evolved in the last decade, with the advent of the association of intraperitoneal chemotherapy, use of chemotherapy in dense dose and the addition of other drugs. Despite the existing treatments, recurrence rates remain high for ovarian cancer, occurring in about 25% of patients with early-stage disease and 80% of those with advanced disease. In this way, there is a need to seek new treatments for this type of cancer. Thus, the main objectives of this study will be characterize the histopathological and molecular effects of OncoTherad and nanostructured phosphate (FO) immunotherapy treatments associated with Platelet Rich Plasma (PRP) in the treatment of chemically induced ovarian cancer in Fischer 344 female mice; and establish the possible mechanisms of action of these therapeutic associations by relating TLRs 2 and 4, in signaling pathways of STAT / JAK1 / JAK2 and RANK / RANKL / OPG; in growth factors PDGF / IGF-1 / TGF-²; and check pathway of immune system PD-1 / PD-L1.

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