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Your search keyword '"Gaudichon, Jérémie"' showing total 6 results
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6 results on '"Gaudichon, Jérémie"'

1. Childhood Langerhans cell histiocytosis hematological involvement: severity associated with BRAFV600Eloads

Author

Thalhammer, Julian, Jeziorski, Eric, Marec-Bérard, Perrine, Barkaoui, Mohamed Aziz, Pagnier, Anne, Rohrlich, Pierre-Simon, Chevallier, Aurore, Carausu, Liana, Aladjidi, Nathalie, Rigaud, Charlotte, Leruste, Amaury, Azarnoush, Saba, Lauvray, Thomas, Le Louet, Solenne, Gandemer, Virginie, Treguier, Pauline, Mansuy, Ludovic, Pasquet, Marlene, Olivier, Laura, Rome, Angélique, Saultier, Paul, Isfan, Fiorentina, Renard, Cécile, Li Thiao Te, Valerie, Salmon, Alexandra, Blanc, Laurence, Abou Chahla, Wadih, Lambilliotte, Anne, Stephan, Jean-Louis, Geissmann, Frederic, Lejeune, Julien, Mallebranche, Coralie, Reguerre, Yves, Grain, Audrey, Thomas, Caroline, Hélias-Rodzewicz, Zofia, Moshous, Despina, Fenneteau, Odile, Coulomb-L’Hermine, Aurore, Lapillonne, Hélène, de Saint-Basile, Geneviève, Emile, Jean-François, Héritier, Sébastien, Donadieu, Jean, Devoldere, Catherine, Gourmel, Antoine, Lutun, Anne, Leglise, Sophie, Pellier, Isabelle, Proust, Stéphanie, Cheikh, Nathalie, Klein, Sébastien, Simon, Pauline, Verite, Cécile, Miaz, Leila, Bodet, Damien, Deparis, Marianna, Gaudichon, Jérémie, Dore, Eric, Kanold, Justyna, Briandet, Claire, Desplantes, Claire, Neuman, Florent, Adjaoud, Dalila, Armari-Alla, Corinne, Plantaz, Dominique, Perret, Cécile, Bruno, Bénedicte, Nelken, Brigitte, Piguet, Christophe, Bertrand, Yves, Garnier, Nathalie, Kebaili, Kamila, Ouachee, Marie, Coze, Carole, Curtillet, Catherine, Gentet, Jean-Claude, Michel, Gérard, Galambrun, Claire, Chastagner, Pascal, Boutroux, Hélène, Landman-Parker, Judith, Bodak, Nathalie, Leverger, Guy, Petit, Arnaud, Simonin, Mathieu, Tabone, Marie-Dominique, Bader-Meunier, Brigitte, Blanche, Stéphane, Castelle, Martin, Neven, Bénédicte, Bodemer, Christine, Perrin, Olivia Boccara, Aerts, Isabelle, Orbach, Daniel, Bourdeaut, Franck, Brugieres, Laurence, Dufour, Christelle, Minard, Véronique, Valteau-Couanet, Dominique, Blanc, Laurence, Millot, Frédéric, Guimard, Grégory, Pluchart, Claire, Bonneau, Jacinthe, Chappe, Céline, Taque, Sophie, Pertuisel, Sophie, Gandemer, Virginie, Probert, Jamie, Puiseux, Chloé, Buchbinder, Nimrod, Dumesnil, Cécile, Filhon, Bruno, Marie-Cardine, Aude, Schneider, Pascale, Berger, Claire, Thouvenin-Doulet, Sandrine, Entz-Werle, Natacha, Paillard, Catherine, Spiegel, Alexandra, Plat, Geneviève, Blouin, Pascale, Jourdain, Anne, Yvert-Guillebert, Marion, Jehanne, Mathilde, Benadiba, Joy, Soler, Christine, Poiree, Maryline, Haouy, Stéphanie, Sirvent, Nicolas, and Saumet, Laure

Abstract

•LCH-HI is life threatening, defined as hemoglobin ≤7 g/dL and/or platelets ≤20 × 109/L.•LCH-HI severity, associated with BRAFV600Evariant and macrophage activation, may require early MAPK inhibitors.

Published
2025
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2. ETV6-RUNX1 and RUNX1 directly regulate RAG1 expression: one more step in the understanding of childhood B-cell acute lymphoblastic leukemia leukemogenesis

Author

Jakobczyk, Hélène, Jiang, Yan, Debaize, Lydie, Soubise, Benoit, Avner, Stéphane, Sérandour, Aurélien A., Rouger-Gaudichon, Jérémie, Rio, Anne-Gaëlle, Carroll, Jason S., Raslova, Hana, Gilot, David, Liu, Ziling, Demengeot, Jocelyne, Salbert, Gilles, Douet-Guilbert, Nathalie, Corcos, Laurent, Galibert, Marie-Dominique, Gandemer, Virginie, and Troadec, Marie-Bérengère

Abstract

ETV6-RUNX1 and RUNX1 directly promote RAG1expression.ETV6-RUNX1 and RUNX1 preferentially bind to the −1200 bp enhancer of RAG1and the −80 bp promoter of RAG1gene respectively, and compete for these bindings.ETV6-RUNX1 and RUNX1 induce an excessive RAG recombinase activity.ETV6-RUNX1 participates directly in two events of the multi-hit ALL leukemogenesis: as an initiating event and as an activator of RAG1expression.

Published
2022
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3. COVID19 and acute lymphoblastic leukemias of children and adolescents: Updated recommendations (Version 2) of the Leukemia Committee of the French Society for the fight against Cancers and leukemias in children and adolescents (SFCE)

Author

Rouger-Gaudichon, Jérémie, Bertrand, Yves, Boissel, Nicolas, Brethon, Benoit, Ducassou, Stéphane, Gandemer, Virginie, Halfon-Domenech, Carine, Leblanc, Thierry, Leverger, Guy, Michel, Gérard, Petit, Arnaud, Ray-Lunven, Anne-France, Rohrlich, Pierre-Simon, Schneider, Pascale, Sirvent, Nicolas, Strullu, Marion, and Baruchel, André

Abstract

Since the emergence of the SARS-CoV-2 infection, many recommendations have been made. However, the very specific nature of acute lymphoblastic leukemias and their treatment in children and adolescents led the Leukemia Committee of the French Society for the fight against Cancers and leukemias in children and adolescents (SFCE) to propose more specific recommendations. Here is the second version of these recommendations updated according to the evolution of knowledge on COVID19.

Published
2021
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4. Mechanisms of extramedullary relapse in acute lymphoblastic leukemia: Reconciling biological concepts and clinical issues.

Author

Gaudichon, Jérémie, Jakobczyk, Hélène, Debaize, Lydie, Cousin, Elie, Galibert, Marie-Dominique, Troadec, Marie-Bérengère, and Gandemer, Virginie

Abstract

Long-term survival rates in childhood acute lymphoblastic leukemia (ALL) are currently above 85% due to huge improvements in treatment. However, 15-20% of children still experience relapses. Relapses can either occur in the bone marrow or at extramedullary sites, such as gonads or the central nervous system (CNS), formerly referred to as ALL-blast sanctuaries. The reason why ALL cells migrate to and stay in these sites is still unclear. In this review, we have attempted to assemble the evidence concerning the microenvironmental factors that could explain why ALL cells reside in such sites. We present criteria that make extramedullary leukemia niches and solid tumor metastatic niches comparable. Indeed, considering extramedullary leukemias as metastases could be a useful approach for proposing more effective treatments. In this context, we conclude with several examples of potential niche-based therapies which could be successfully added to current treatments of ALL. [ABSTRACT FROM AUTHOR]

Published
2019
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5. Complete and Repeated Response of a Metastatic ALK-rearranged Inflammatory Myofibroblastic Tumor to Crizotinib in a Teenage Girl

Author

Gaudichon, Jérémie, Jeanne-Pasquier, Corinne, Deparis, Marianna, Veyssière, Alexis, Heyndrickx, Maxime, Minckes, Odile, and Orbach, Daniel

Abstract

Supplemental Digital Content is available in the text.Inflammatory myofibroblastic tumors (IMT) are rare tumors in children and young adults, considered by the World Health Organization to be intermediate malignancies and rarely metastasizing, with the presence of an anaplastic lymphoma kinase rearrangement in about 50% of the cases. We report the case of a teenager who presented with a metastatic aggressive IMT that was life-threatening despite multiple treatments, and which responded repeatedly to anaplastic lymphoma kinase–targeted crizotinib therapy. Crizotinib induced drastic primary tumor regression, which was sufficient to allow surgical resection and to control distant disease. This case shows that crizotinib is a promising therapy in IMT, even in adolescents and young adults.

Published
2016
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6. CBFA2T3 Enhances Transcriptional Activity of RUNX1: Implication in Leukemia

Author

Jakobczyk, Hélène, Debaize, Lydie, Rio, Anne-Gaëlle, Gaudichon, Jérémie, Serandour, Aurélien, Avner, Stéphane, Delalande, Olivier, Salbert, Gilles, Galibert, Marie-Dominique, Gandemer, Virginie, and Troadec, Marie-Berengere

Abstract

Pre-B acute lymphoblastic leukemia (BCP-ALL) is the most common type of pediatric cancer. Many expression-profiling studies have uncovered genes deregulated in BCP-ALL compared to normal pre-B cells. Yet, the roles of the deregulation of those genes in the onset and maintenance of BCP-ALL are still unclear. We were interested in two genes, CBFA2T3(Core-Binding Factor, Runt Domain, Alpha Subunit 2; Translocated To, 3) and RUNX1(Runt Related Transcription Factor 1), which are specifically overexpressed in BCP-ALL characterized by the presence of ETV6-RUNX1fusion gene. CBFA2T3 is a hematopoietic corepressor. Alteration of its function is implicated in leukemia. RUNX1 is a transcription factor, whose activation or repression activity depends on cofactors. RUNX1 deregulation is also involved in many hematological disorders. Our goal was to explore the role of these two genes in BCP-ALL. We demonstrated the major role of CBFA2T3 in the control of RUNX1 activity.

Published
2017
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