CD36 drives metastasis and relapse in acute myeloid leukemia

Understanding the mechanisms of relapse is a major challenge in effectively treating cancer. In the case of acute myeloid leukemia (AML), researchers from the Cancer Research Center of Toulouse and Restore have discovered that a protein called CD36 plays a significant role.

They studied a group of 1,273 AML patients and found that CD36 was associated with the spread of cancer cells outside the bone marrow, an increased risk of relapse after intensive chemotherapy, and reduced overall survival.

Contrary to previous knowledge, CD36 is not necessary for the utilization of lipids by cancer cells. Instead, it promotes their migration by binding to another molecule called thrombospondin-1. After chemotherapy, CD36-expressing cancer cells become more prevalent and exhibit a phenotype similar to cellular aging while maintaining their ability to move.

In mouse models, the researchers also observed that inhibiting CD36 reduced the spread of cancer cells and prolonged the survival of chemotherapy-treated mice.

These findings suggest that CD36 could be used as an independent marker of poor prognosis in AML patients and represent a promising target for improving the treatment of this disease.

CD36 could be used to better study extramedullary disease (metastases) in AML, especially since CD36 is routinely analyzed in many biological laboratories for this cancer. A company based in Barcelona is currently developing a CD36 inhibitor for clinical trial, we hope to expand its application to AML.

Collaborations and acknowledgements

Funding :

• Fondation Toulouse Cancer Santé
• Fondation ARC pour la recherche sur le cancer
• Ligue contre le cancer
• ANR (Agence nationale de la recherche)
• Association Gaël Adolescent Espoir Leucémie
• Institut national du cancer
• Université Paul Sabatier Toulouse III
• IUCT-Oncopole
• CHU de Toulouse
• Inserm
• CNRS
• EFS
• ENVT

Collaborations

CRCM (Remy Castellano et Yves Collette), I2MC (Camille Bergoglio et Cédric Moro),