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Immunophenotypic characterization of NK cells in a Flt3-Tet2 murine model of Acute Myeloid Leukemia

Grant number: 23/12667-1
Support Opportunities:Scholarships in Brazil - Scientific Initiation
Effective date (Start): February 01, 2024
Effective date (End): January 31, 2025
Field of knowledge:Health Sciences - Medicine - Medical Clinics
Principal Investigator:Lorena Lôbo de Figueiredo Pontes
Grantee:Emmanuel Victor Barbosa Ferreira
Host Institution: Hemocentro de Ribeirão Preto. Hospital das Clínicas da Faculdade de Medicina de Ribeirão Preto da USP (HCMRP). Secretaria da Saúde (São Paulo - Estado). Ribeirão Preto , SP, Brazil
Associated research grant:21/06841-3 - Molecular and phenotypical mechanisms driving immune evasion in myeloid malignancies, AP.JP2


Acute Myeloid Leukemia (AML) is a hematological disease characterized by a malignant clonal alteration that affects the bone marrow due to the proliferation and expansion of leukemia stem cells (LSCs) of myeloid lineage that undergo a blockage in their differentiation, thereby impairing normal hematopoiesis, resulting in cases of anemia, granulocytopenia, or thrombocytopenia. The proliferative advantage of LSCs is attributed to genetic mutations occurring in the normal hematopoietic stem cell (HSC), among which mutations in the FLT3 gene are recurrent and associated with a worse prognosis. AML blasts play a crucial role in immune evasion by modulating the marrow microenvironment, primarily through immunosuppressive activity, characterized by the accumulation of regulatory cells, such as regulatory T lymphocytes (Tregs), and the presence of myeloid-derived suppressor cells (MDSCs) that protect leukemia blasts. Previously published data from our research group demonstrate a decrease in the frequency of total and cytotoxic NK cells in patients diagnosed with AML, especially in AML with FLT3-ITD mutation, emphasizing the need to understand the immune dysfunction seen in AML with this genetic alteration and to elucidate the mechanisms that contribute to the resistance of this leukemia. Therefore, we propose the immunophenotypic evaluation of NK cells using the murine model Flt3-ITDki/Mx1-Tet2f/f, which resembles AML presented in humans. In this way, we hope to generate results that will enhance the understanding of the immune dysfunction observed in cases of AML with FLT3-ITD mutation.

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