| Grant number: | 14/04234-9 |
| Support Opportunities: | Scholarships in Brazil - Doctorate |
| Start date: | December 01, 2014 |
| End date: | August 31, 2018 |
| Field of knowledge: | Health Sciences - Medicine |
| Agreement: | Coordination of Improvement of Higher Education Personnel (CAPES) |
| Principal Investigator: | Fabíola Attié de Castro |
| Grantee: | Maira da Costa Cacemiro |
| Host Institution: | Faculdade de Ciências Farmacêuticas de Ribeirão Preto (FCFRP). Universidade de São Paulo (USP). Ribeirão Preto , SP, Brazil |
| Associated scholarship(s): | 16/03265-3 - Study of CALR del52 and ins5 knock-in mouse models and comparison to the JAK2V617F knock-in mouse model, BE.EP.DR |
Abstract Chronic myeloproliferative neoplasms (CMPN) are haematological disease characterized by the increase of mature hematopoietic cells of one or more of the myeloid series (granulocyte, erythrocyte , megakaryocyte or mast cells) proliferation. Among the CMPN we will investigate the polycythemia vera (PV), essential thrombocythemia (ET) and primary myelofibrosis (MF).CMPN may present the JAK2V617F mutation which occurs in 95 % of PV patients and 50% of ET and MF patients. The JAK2V617F mutation constitutively active STAT3 transducer protein, which is related to apoptosis resistance and myeloproliferation in these diseases. Although all the molecular knowledge about CMPN pathogenesis, these diseases do not have a efficient therapy. Thus, more studies to better understand their pathophysiology and description of new therapeutic targets, as the molecules via the HIPPO / LATS are needed.This study will investigate the relationship between apoptosis impairment and the Hippo-LATS pathway deregulation in PV, ET and MF patients. The gene expression of Hippo-LATS pathway members will be quantify in CMPN patients leukocytes, Hel.92.1.7 and SET 2 cell lines treated or untreated with JAK2 inhibitors. (AU) | |
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