Emilie Leroy

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Ligand binding to the extracellular domain of the thrombopoietin receptor (TpoR) imparts a specific orientation on the transmembrane (TM) and intracellular domains of the receptors that is required for physiologic activation via receptor dimerization. To map the inactive and active dimeric orientations of the TM helices, we performed asparagine(More)
The main molecular basis of essential thrombocythemia and hereditary thrombocytosis is acquired, and germ-line-activating mutations affect the thrombopoietin signaling axis. We have identified 2 families with hereditary thrombocytosis presenting novel heterozygous germ-line mutations of JAK2. One family carries the JAK2 R867Q mutation located in the kinase(More)
LTHOUGH leukemic infiltrations of the heart are often encountered, particularly in the stem cell and myelogenous types ofleukemia,’ little attention in the literature has been given to their clinical recognition. Cardiac manifestations, almost always first discovered at necropsy, have been considered to be a part of the protean nature of the leukemic(More)
We retrospectively evaluated the initial site of bone lesions in 200 patients with Paget's disease. There were 117 males and 83 females. Mean follow-up was 13 years in 98 patients. The initial site can be determined accurately only if less than one third of the bone is involved. Paget's disease usually begins in the cancellous bone of an epiphysis or(More)
The role of somatic JAK2 mutations in clonal myeloproliferative neoplasms (MPNs) is well established. Recently, germ line JAK2 mutations were associated with polyclonal hereditary thrombocytosis and triple-negative MPNs. We studied a patient who inherited 2 heterozygous JAK2 mutations, E846D from the mother and R1063H from the father, and exhibited(More)
Essential thrombocythemia (ET) and primary myelofibrosis (PMF) are chronic diseases characterized by clonal hematopoiesis and hyperproliferation of terminally differentiated myeloid cells. The disease is driven by somatic mutations in exon 9 of CALR or exon 10 of MPL or JAK2-V617F in >90% of the cases, whereas the remaining cases are termed "triple(More)
The JAK3 tyrosine kinase is mutated in 10 to 16% of T-cell acute lymphoblastic leukemia (T-ALL) cases. JAK3 mutants induce constitutive JAK/STAT signaling and cause leukemia when expressed in the bone marrow cells of mice. Surprisingly, we observed that one third of the JAK3 mutant T-ALL cases harbor two JAK3 mutations, some of which are mono-allelic and(More)
The acquisition of growth signal self-sufficiency is 1 of the hallmarks of cancer. We previously reported that the murine interleukin-9-dependent TS1 cell line gives rise to growth factor-independent clones with constitutive activation of the Janus kinase (JAK)- signal transducer and activator of transcription (STAT) pathway. Here, we show that this(More)