American Association for Cancer Research
can-22-3682_supplementary_data_suppsf1.pdf (540.66 kB)

Supplementary Data from CD36 Drives Metastasis and Relapse in Acute Myeloid Leukemia

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journal contribution
posted on 2023-09-01, 08:22 authored by Thomas Farge, Jean Nakhle, Damien Lagarde, Guillaume Cognet, Nathaniel Polley, Rémy Castellano, Marie-Laure Nicolau, Claudie Bosc, Marie Sabatier, Ambrine Sahal, Estelle Saland, Yannick Jeanson, Nathan Guiraud, Emeline Boet, Camille Bergoglio, Mathilde Gotanègre, Pierre-Luc Mouchel, Lucille Stuani, Clément Larrue, Marie Sallese, Véronique De Mas, Cedric Moro, Cédric Dray, Yves Collette, Isabelle Raymond-Letron, Isabelle Ader, Christian Récher, Jean-Emmanuel Sarry, Florence Cabon, François Vergez, Audrey Carrière

Figure S1


Institut National Du Cancer (INCa)

Investissement d'Avenir PSPC

Laboratoire d'Excellence Toulouse Cancer

Fondation Toulouse Cancer Santé (Toulouse Cancer Health Foundation)

Fondation ARC pour la Recherche sur le Cancer (ARC)

Canceropole Grand Sud Ouest

Ligue Nationale Contre le Cancer

Association Prolific

Association GAEL

European Regional Development Fund Interreg V-A Spain France Andorra (POCTEFA)

Agence Nationale de la Recherche - Investissement d'avenir

Agence Nationale de la Recherche (ANR)



Identifying mechanisms underlying relapse is a major clinical issue for effective cancer treatment. The emerging understanding of the importance of metastasis in hematologic malignancies suggests that it could also play a role in drug resistance and relapse in acute myeloid leukemia (AML). In a cohort of 1,273 AML patients, we uncovered that the multifunctional scavenger receptor CD36 was positively associated with extramedullary dissemination of leukemic blasts, increased risk of relapse after intensive chemotherapy, and reduced event-free and overall survival. CD36 was dispensable for lipid uptake but fostered blast migration through its binding with thrombospondin-1. CD36-expressing blasts, which were largely enriched after chemotherapy, exhibited a senescent-like phenotype while maintaining their migratory ability. In xenograft mouse models, CD36 inhibition reduced metastasis of blasts and prolonged survival of chemotherapy-treated mice. These results pave the way for the development of CD36 as an independent marker of poor prognosis in AML patients and a promising actionable target to improve the outcome of patients. CD36 promotes blast migration and extramedullary disease in acute myeloid leukemia and represents a critical target that can be exploited for clinical prognosis and patient treatment.

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