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CCBIO seminar series

CCBIO Seminar – Antonio Curti CANCELLED

THIS SEMINAR IS UNFORTUNATELY CANCELLED DUE TO ILLNESS Welcome to the CCBIO seminar series in the spring term of 2024. Open to all in auditorium 4, BBB. No registration necessary. Speaker is Antonio Curti, Bologna, with the topic “Driver mutations and immune microenvironment in acute myeloid leukemia (AML)”.

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THIS SEMINAR IS UNFORTUNATELY CANCELLED DUE TO ILLNESS 

SpeakerAntonio Curti, University Hospital Sant’Orsola-Malpighi, Institute of Hematology “Seràgnoli”, Bologna, Italy
Title: Driver mutations and immune microenvironment in acute myeloid leukemia (AML)
Host: Bjørn Tore Gjertsen
Where: Auditorium 4, BB-building
When: May 30, 2024 at 14.30-15.30

No registration necessary. 

Abstract: Acute myeloid leukemia (AML) is a heterogeneous clonal disease deriving from a rare population of bone marrow leukemic stem cells. Although new and potent drugs have recently entered the clinical stage, the 5-year patient overall survival is largely unsatisfactory, reaching 30% and dropping to 5-10% in the elderly. Therefore, there is an urgent and unmet need for effective new treatment modalities for AML. In the last years, cancer immunotherapy is gaining much interest due to its unique characteristics, such as the absence of conventional drug resistance mechanisms and low grade of toxicity. In AML, the immunotherapy field is evolving and expanding. However, despite a strong rationale, clinical results have not been satisfactory, and several questions need to be answered for a full exploitation of immune interventions in AML. Among them, the immunological effects of intrinsic driver AML gene mutations on the immune microenvironment and their relevance for immunotherapy are still poorly investigated. Based on these premises, the aim of the talk is to move from the current state of art of immunotherapy in AML and discuss recent biological findings, which strongly indicate the specificity of bone marrow immune microenvironment as a critical issue for an effective biology-driven development of immunotherapies in AML. In that, the contribution of cell intrinsic driver mutations, such as FLT3 and TP53, in dictating the adaptation and changes in immune microenvironment, especially at the metabolic level, will be discussed by showing unpublished results of the group.