Séverine Cathelin

This study identifies CD59 as a critical regulator of Ras-MAPK signaling in AML, showing its depletion impairs leukemic growth and identifies rILYd4 as a potential therapeutic target.

This study identifies MBD1-L, an aberrantly spliced transcript in MDS, which drives epigenetic changes leading to myeloerythroid defects, and shows ASO-based targeting can restore erythroid differentiation.

This study identifies stress granules as critical for AML stem cell survival and stress adaptation, revealing their role in gene regulation and potential as therapeutic targets.