Abstract

Myelofibrosis (MF) are a non-BCR-ABL myeloproliferative neoplasms (NMPs) associated with poor outcomes. Current treatment has little effect on the natural history of the disease. MF results from complex interactions between 1) the malignant clone, 2) an inflammatory context, and 3) remodeling of the bone marrow (BM) microenvironment. Each of these points is a potential target of PPAR-y activation. Here, we demonstrated the therapeutic potential of PPAR-y agonists in resolving MF in three mouse models. We showed that PPAR-y agonists reduce myeloproliferation, modulate inflammation, and protect the BM stroma in vitro and ex vivo. Activation of PPAR-y constitutes a relevant therapeutic target in MF and our data support the possibility of using PPAR-y agonists in clinical practice.

Authors

Juliette Lambert, Joseph Saliba, Carolina Calderon, Karine Sii-Felice, Mohammad Salma, Valérie Edmond, Jean-Claude Alvarez, Marc Delord, Caroline Marty, Isabelle Plo, Jean-Jacques Kiladjian, Eric Soler, William Vainchenker, Jean-Luc Villeval, Philippe Rousselot, Stephane Prost

×

Download this citation for these citation managers:

Or, download this citation in these formats:

If you experience problems using these citation formats, send us feedback.

Advertisement