Postdoctoral Fellow

Constance Delwarde

Profile

I completed my PhD on cardiovascular research, in Nantes University (France), which was awarded the 2022 best fundamental research thesis from the French Society of Cardiology.

I pursued my career with a first postdoc in Boston (USA), at the Center for Interdisciplinary Cardiovascular Sciences, Harvard, where I strengthened my skills on vascular biology, macrophages, and lipids, in atherosclerosis.

I am very glad and happy to become a Marie Curie Josep Carreras Research Fellow at the IJC, working on the role of endothelial cell in non-Hodgkin B-cell lymphoma.

Project description

ENDOFEN stems from a collaborative effort to explore the emerging subpopulation of fenestrated endothelial cells (ECs) with inflammatory properties, characterized by elevated expression of Plvap, in the context of non-Hodgkin lymphoma (NHL). This project builds on my longstanding interest in the convergence of cardiovascular research and immuno-oncology. Through ENDOFEN, I aim to examine the role of these fenestrated ECs in regulating inflammation and promoting immune cellEC interactions during lymphoma progression and metastasis, particularly in relation to chemotherapy-induced effects. The primary hypothesis of ENDOFEN is that ECs are reprogrammed into a fenestrated phenotype during cancer progression, which facilitates immune infiltration and metastasis. My approach will focus on NHL, as it is well-known that the standard treatment (R-CHOP therapy) increases the risk of metastasis, and a significant proportion of NHL patients experience relapse. Therefore, I aim to explore how fenestrated ECs influence vascular inflammation and how targeting these cells may help prevent metastasis and improve outcomes for NHL patients’ post-chemotherapy. Through four specific aims, I will study the dynamics of EC fenestration during NHL metastasis (Aim 1), assess chemotherapy’s impact on EC fenestration (Aim 2), investigate immune-EC interactions (Aim 3), and test the therapeutic potential of targeting fenestrated ECs to reduce vascular inflammation and metastasis (Aim 4). Utilizing novel mouse models (e.g., Plvap-CreERT2), cuttingedge imaging techniques, and state-of-the-art -omics technologies, I will generate a comprehensive map of the role of fenestrated ECs in NHL progression. Ultimately, this research may lead to new therapeutic strategies targeting EC subsets to reduce inflammation and prevent metastasis relapse upon chemotherapy treatment.