C
Chloé James
Researcher at University of Bordeaux
Publications - 92
Citations - 8034
Chloé James is an academic researcher from University of Bordeaux. The author has contributed to research in topics: Medicine & Myelofibrosis. The author has an hindex of 24, co-authored 74 publications receiving 7446 citations. Previous affiliations of Chloé James include Institut Gustave Roussy & Walter and Eliza Hall Institute of Medical Research.
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Journal ArticleDOI
A unique clonal JAK2 mutation leading to constitutive signalling causes polycythaemia vera
Chloé James,Valérie Ugo,Jean-Pierre Le Couedic,Judith Staerk,François Delhommeau,Catherine Lacout,Loïc Garçon,Hana Raslova,Roland Berger,Annelise Bennaceur-Griscelli,Jean-Luc Villeval,Stefan N. Constantinescu,Nicole Casadevall,William Vainchenker +13 more
TL;DR: A clonal and recurrent mutation in the JH2 pseudo-kinase domain of the Janus kinase 2 (JAK2) gene in most (> 80%) polycythaemia vera patients leads to constitutive tyrosine phosphorylation activity that promotes cytokine hypersensitivity and induces erythrocytosis in a mouse model.
Journal ArticleDOI
Mutation in TET2 in Myeloid Cancers
François Delhommeau,Sabrina Dupont,Véronique Della Valle,Chloé James,Séverine Trannoy,Aline Massé,Olivier Kosmider,Jean-Pierre Le Couedic,Fabienne Robert,Antonio José Alberdi,Yann Lécluse,Isabelle Plo,François Dreyfus,Christophe Marzac,Nicole Casadevall,Catherine Lacombe,Serge Romana,Philippe Dessen,Jean Soulier,Franck Viguié,Michaela Fontenay,William Vainchenker,Olivier Bernard +22 more
TL;DR: Somatic mutations in TET2 occur in about 15% of patients with various myeloid cancers and were present in hematopoietic stem cells and preceded the JAK2 V617F mutation in the five samples from patients with myeloproliferative disorders that were analyzed.
Journal ArticleDOI
A unique clonal JAK2 mutation leading to constitutive signalling causes polycythaemia vera
TL;DR: A clonal and recurrent mutation in the JH2 pseudo-kinase domain of the Janus kinase 2 (JAK2) gene in most (> 80%) polycythaemia vera patients leads to constitutive tyrosine phosphorylation activity that promotes cytokine hypersensitivity and induces erythrocytosis in a mouse model.
Journal ArticleDOI
The JAK2 617V>F mutation triggers erythropoietin hypersensitivity and terminal erythroid amplification in primary cells from patients with polycythemia vera.
Sabrina Dupont,Aline Massé,Chloé James,Irène Teyssandier,Yann Lécluse,Frédéric Larbret,Valérie Ugo,Patrick Saulnier,Serge Koscielny,Jean Pierre Le Couédic,Nicole Casadevall,Nicole Casadevall,William Vainchenker,François Delhommeau,François Delhommeau +14 more
TL;DR: The results suggest that, for PV, erythrocytosis can occur through two mechanisms: terminal erythroid amplification triggered by JAK2 617V>F homozygosity, and a 2-step process including the upstream amplification of heterozygous cells that may involve additional molecular events.
Journal ArticleDOI
Megakaryocytes possess a functional intrinsic apoptosis pathway that must be restrained to survive and produce platelets
Emma C. Josefsson,Chloé James,Katya J. Henley,Marlyse A. Debrincat,Marlyse A. Debrincat,Kelly L. Rogers,Kelly L. Rogers,Mark R. Dowling,Mark R. Dowling,Michael J. White,Michael J. White,Elizabeth A. Kruse,Elizabeth A. Kruse,Rachael M. Lane,Sarah Ellis,Paquita Nurden,Kylie D. Mason,Kylie D. Mason,Lorraine A. O'Reilly,Lorraine A. O'Reilly,Andrew W. Roberts,Andrew W. Roberts,Donald Metcalf,Donald Metcalf,David C.S. Huang,David C.S. Huang,Benjamin T. Kile,Benjamin T. Kile +27 more
TL;DR: Deletion of Bak and Bax, the effectors of mitochondrial apoptosis, does not affect platelet production, however, loss of prosurvival Bcl-xL results in megakaryocyte apoptosis and failure of platelet shedding.