CV Science

Alexandre Guy Assistant professor

Course and current status

After first years of medical school at the University of Clermont-Ferrand (France), I realized an intersnhip in Internal Medicine at the University of Bordeaux (2011-2019), with a particular interest in Hematology and Hemostasis. I have defended my medical thesis in 2015 and my degree of specialisation in Internal Medicine in 2019. Regarding my scientific course, I realized a master degree in Paris (University of Paris) with a specialization in hematology (2013-2014). I realized a PhD in Pr Chloé James's lab based in the INSERM Unit 1034 "Biology of cardiovascular diseases" (Bordeaux, France) and defended my PhD in 2018. I then did a post-doctoral fellowship in Radek Skoda's lab from 2020 to 2021 (Basel, Switzerland). From September 2023, I'm assistant professor in Hematology in the Laboratory of Hematology of Bordeaux University Hospital with a research activity in the INSERM Unit "Biology of cardiovascular diseases" in the team "Endothelial cells and thrombosis" headed by Pr Chloé James. My clinical activity in the Laboratory of Hematology is shared betwenn patients's consultations, report of biological results and clinical advices in hemostasis to other departments.

Scientific summary

During my PhD, I worked on the physiopathology of thrombosis during myeloproliferative neoplasms. My first axis of work was to study the role of JAK2V617F mutated endothelial cells in its physiopathology. We were able to demonstrate, using endothelial-specific mouse models, that JAK2V617F mutated ECs participate in the physiopathology of thrombosis during these diseases, notably via an increased adhesion of leuckocytes at the surface of ECs (Guy et al., Haematologica, 2019). Other axis of work, I studied the role of neutrophils and neutrophil extracellular traps in the physiopathology of thrombosis during MPN. Interestingly, we observed that MPN patients do have an increased formation of NET, and that patients with a previous history of thrombosis form more NET that patients without thrombosis. These results suggest that NETosis participates in the physiopathology of thrombosis during MPN (Guy et al., Leukemia, 2020). I then realized 18 months in Radek Skoda's lab in Basel, to study NETosis in the the context of myelofibrosis. During this post-doctoral stay, I also studied the role of platelets in the occurence of thrombosis during JAK2V617F MPN. To elucidate the mechanisms of increased NETosis in JAK2V617F+ MPN, we recently conducted a study using two different mouse models and demonstrated that the collaboration between platelets and neutrophils is crucial for the increased NETosis (Guy et al., J Thromb Haemost, 2023).