| Grant number: | 19/09419-0 |
| Support Opportunities: | Scholarships in Brazil - Doctorate |
| Start date: | January 01, 2021 |
| End date: | January 31, 2024 |
| Field of knowledge: | Health Sciences - Medicine - Pathological Anatomy and Clinical Pathology |
| Principal Investigator: | Fernanda Viviane Mariano Brum Corrêa |
| Grantee: | João Figueira Scarini |
| Host Institution: | Faculdade de Ciências Médicas (FCM). Universidade Estadual de Campinas (UNICAMP). Campinas , SP, Brazil |
| Associated research grant: | 15/07304-0 - Study of genetic and metabolic changes of pleomorphic adenoma and carcinoma ex pleomorphic adenoma by exome, gene expression and immunohistochemistry, AP.JP |
| Associated scholarship(s): | 21/12567-1 - Validation of potential genomic alterations found during the malignant transformation of the pleomorphic adenoma, BE.EP.DR |
Abstract Among the tumors that can affect the salivary glands, two entities constitute interesting models for the study of the mechanism of malignant transformation. The first one, the most common benign tumor in the salivary gland, Pleomorphic Adenoma (PA), may undergo genetic transformations resulting in its malignant counterpart, Carcinoma Ex Pleomorphic Adenoma (CXPA). The latter is a rare and aggressive neoplasm, with metastasis and death in a large percentage of the cases. Although both tumors present important findings from a genetic point of view, the alterations found are focal and in specific gene sites, leaving many doubts about diagnostic markers, pathogenesis, and target therapy of PA and CXPA. In this project, we will study a group of PA and CXPA (subdivided as to the histological type and degree of progression) through the complete sequencing of the exome (Whole Exome Sequencing - WES) and we will complement the findings with previous results of our group that was performed with the CGH-array technique. In this way, we hope to expand individual genetic knowledge about PA and CXPA and still be able to compare not only the changes in the number of copies and mutations acquired in the benign counterpart and which are preserved in the carcinoma but also the particular changes to the malignant tumor. Furthermore, by analyzing genetic alterations related to PA tumorigenesis and CXPA tumor progression, we intend to add significant knowledge to what is currently known about these tumors and also to be able to provide information on diagnostic markers, pathogenesis, and target therapy, which will later be reflected in instruments for clinical application and prognostic improvement of patients affected by these neoplasms. (AU) | |
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