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    The origins of acute myeloid leukemia: genetic predispositions and age-related clonal hematopoiesis

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    Seminar Institut Cochin

    Thursday 23 April 2020 - 12:00 - Room conference Rosalind Franklin, 2nd floor

     

    François Delhommeau
    François Delhommeau

    Laboratoire d’Hématologie Cellulaire HUEP,
    Laboratoire de Médecine Génomique APHP.6 (Oncohématologie)
    Sorbonne Université CRSA UMRS938, Hôpital Saint-Antoine, Paris

     

     invited by Romain Fontaine

    Institut Cochin, 22 rue Méchain, 75014 Paris

     

    Abstract

    Acute myeloid leukemia (AML) is a clinically and genetically heterogeneous group of blood cancers.  Our understanding of the origins of AML results from recent studies that addressed their clonal hierarchy and the biology of normal and malignant hematopoietic stem cells. Several conditions such as aging or genetic diseases predispose to pre-leukemic states that can evolve to distinct types of AML. Our group studies the genetic events that lead to the initiation of pre-leukemic clones, and then to AML. In the context of genetic diseases with increased risk of AML, we are focused on the early emergence of mutant clones in congenital neutropenia (Shwachman Diamond and GATA2 syndromes). Regarding adult AML without genetic predisposition, we study the most frequent age-related pre-leukemic mutations (TET2, DNMT3A, and TP53 mutations). Our goal is to understand how these acquired lesions can provide a selective advantage to mutant cells over normal hematopoietic cells, and then an increased probability for a clonal evolution to AML. Overall, our data indicate that the first pre-leukemic mutations will dictate, through distinct modifications of the crosstalk between hematopoietic stem cells and their micro-environment, the selection of distinct subsequent clonal events, leading to various type of AMLs.

     

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