Équipe
CARINE JOFFRE / MARGHERITA GHISI
ADAPTAML :
Mécanismes d’adaptation non génétiques et résistance
à la thérapie dans les leucémies aigües myéloïdes.
Les spécificités
de notre axe de recherche
Les leucémies aiguës myéloïdes sont des cancers très agressifs avec un taux de survie à 5 ans qui reste faible (moins de 30%). Une meilleure compréhension de la biologie des LAM ainsi que l’identification de nouvelles vulnérabilités moléculaires et cellulaires sont donc essentielles pour développer de nouvelles stratégies thérapeutiques et ainsi améliorer le pronostic des patients.
Pendant de nombreuses années, l’acquisition d’altérations génétiques séquentielles a été considérée comme la cause principale de l’apparition du cancer et de la résistance à la thérapie. Cependant, il est de plus en plus reconnu que des mécanismes non génétiques d’adaptation impliquant un dialogue dynamique entre les cellules cancéreuses et leur microenvironnement jouent un rôle clé à la fois dans le processus de tumorigénèse et dans l’acquisition de résistance aux thérapies anticancéreuses. Or la compréhension de la mise en place de ces mécanismes non génétiques d’adaptation est encore très limitée et représente un domaine de recherche émergeant et prometteur sur lesquels se focalise notre équipe de recherche.
Plus spécifiquement, nos études portent sur le rôle de l’autophagie, de la quiescence et de la régulation épigénétique/post-transcriptionnelle de l’expression des gènes dans la progression de la leucémie, de la résistance aux thérapies et de la rechute, en tenant compte de l’interaction entre les blastes leucémiques et leur microenvironnement.
Pour répondre à ces questions, nous combinons des modèles de LAM in vitro and in vivo cliniquement relevant, (e.g. des xénogreffes de LAM humaines dérivées de patients et de lignées cellulaires (PDX et CLDX) et des modèles de souris transgéniques), avec diverses approches -omiques (séquençage de l’ARN global et à l’échelle de la cellule unique), ATACseq, iCLIP, protéomique, métabolomique) ainsi que des criblages génétiques et pharmacologiques fonctionnels.
Nos travaux, nous l’espérons, servirons de rationnel pour concevoir de nouvelles stratégies thérapeutiques, plus efficaces, afin d’améliorer la prise en charge des patients atteints de LAM.
Leucémies aigües Myéloïdes,
Adaptation,
Hématopoïèse,
Résistance,
Autophagie,
Épissage alternatif,
Microenvironnement,
Cellules Souches,
Quiescence,
Épigénétique.
DES PROJETS
DE RECHERCHE
Étude de la régulation de la quiescence et de son rôle dans la réponse à la chimiothérapie dans la LAM
Clément Larrue
Rôle de la régulation épigénétique et de l’épissage de l’ARN dans la résistance à la thérapie et la biologie de la LAM
Margherita Ghisi
Contribution de l’autophagie de l’hôte à la régulation de l’hématopoïèse dans des conditions normales et pathologiques.
Laura Poillet
Nouvelles fonctions de l’autophagie régissant l’adaptation thérapeutique dans la LAM
Carine Joffre
LES FOCUS
DE L’ÉQUIPE
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PRODUCTIONS SCIENTIFIQUES
PUBLICATIONS 2026
7813506
P5EV42SF
2026
1
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60091
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https://www.crct-inserm.fr/wp-content/plugins/zotpress/
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Larrue, Clement, Sarah Mouche, Paolo Angelino, Maxime Sajot, Rudy Birsen, Olivier Kosmider, Thomas Mckee, et al. “Targeting Ferritinophagy Impairs Quiescent Cancer Stem Cells in Acute Myeloid Leukemia in Vitro and in Vivo Models.” Science Translational Medicine 16, no. 757 (July 24, 2024): eadk1731. https://doi.org/10.1126/scitranslmed.adk1731.
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Courdy, Charly, Loïc Platteeuw, Charlotte Ducau, Isabelle De Araujo, Emeline Boet, Ambrine Sahal, Estelle Saland, et al. “Targeting PP2A-Dependent Autophagy Enhances Sensitivity to Ruxolitinib in JAK2V617F Myeloproliferative Neoplasms.” Blood Cancer Journal 13, no. 1 (July 10, 2023): 106. https://doi.org/10.1038/s41408-023-00875-x.
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Joffre, Carine, Charlotte Ducau, Laura Poillet-Perez, Charly Courdy, and Véronique Mansat-De Mas. “Autophagy a Close Relative of AML Biology.” Biology 10, no. 6 (June 18, 2021): 552. https://doi.org/10.3390/biology10060552.
Bosc, Claudie, Estelle Saland, Aurélie Bousard, Noémie Gadaud, Marie Sabatier, Guillaume Cognet, Thomas Farge, et al. “Mitochondrial Inhibitors Circumvent Adaptive Resistance to Venetoclax and Cytarabine Combination Therapy in Acute Myeloid Leukemia.” Nature Cancer 2, no. 11 (2021): 1204–23. https://doi.org/10.1038/s43018-021-00264-y.
PUBLICATIONS 2020
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2020
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Bosc, Claudie, Nicolas Broin, Marjorie Fanjul, Estelle Saland, Thomas Farge, Charly Courdy, Aurélie Batut, et al. “Autophagy Regulates Fatty Acid Availability for Oxidative Phosphorylation through Mitochondria-Endoplasmic Reticulum Contact Sites.” Nature Communications 11, no. 1 (August 13, 2020): 4056. https://doi.org/10.1038/s41467-020-17882-2.
Aroua, Nesrine, Emeline Boet, Margherita Ghisi, Marie-Laure Nicolau-Travers, Estelle Saland, Ryan Gwilliam, Fabienne de Toni, et al. “Extracellular ATP and CD39 Activate cAMP-Mediated Mitochondrial Stress Response to Promote Cytarabine Resistance in Acute Myeloid Leukemia.” Cancer Discovery, July 8, 2020, CD-19-1008. https://doi.org/10.1158/2159-8290.CD-19-1008.
PUBLICATIONS 2019
7813506
P5EV42SF
2019
1
chicago-fullnote-bibliography
50
date
desc
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Larrue, Clément, Quentin Heydt, Estelle Saland, Héléna Boutzen, Tony Kaoma, Jean-Emmanuel Sarry, Carine Joffre, and Christian Récher. “Oncogenic KIT Mutations Induce STAT3-Dependent Autophagy to Support Cell Proliferation in Acute Myeloid Leukemia.” Oncogenesis 8, no. 8 (July 16, 2019): 39. https://doi.org/10.1038/s41389-019-0148-9.
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Heydt, Q., C. Larrue, E. Saland, S. Bertoli, J.-E. Sarry, A. Besson, S. Manenti, C. Joffre, and V. Mansat-De Mas. “Oncogenic FLT3-ITD Supports Autophagy via ATF4 in Acute Myeloid Leukemia.” Oncogene 37, no. 6 (08 2018): 787–97. https://doi.org/10.1038/onc.2017.376.
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