Current lab members:

• Jean Albrengues, PhD — CRCN INSERM
• Hussein Issaoui, post-doc
• Lola Bellone, PhD Student
• Caroline Jeanneau, Engineer (IR)
• Isabelle Bourget,Engineer
• Aurelia Errante, Technician

Lab Alumni:

• Alexandra Mousset, PhD — Université Côte d’Azur
• Victor Ferreira (Erasmus Master Student, Federal University of Rio de Janeiro)
• Loan Tran, Engineer (IE)

Inflammation is a fundamental physiological process that ensures tissue repair, host defense, and the maintenance of tissue homeostasis. When tightly regulated, inflammatory responses promote healing and restore normal tissue function. By contrast, chronic or dysregulated inflammation is a key driver of multiple pathological conditions, including cancer, chronic inflammatory diseases, tissue remodeling disorders, and fibrosis. Aging is accompanied by a gradual increase in basal inflammatory tone—termed inflammaging—which synergizes with chronic inflammatory insults to promote tissue dysfunction, fibrosis, and cancer. While inflammation is clearly linked to malignant transformation and progression, as well as degenerative processes, the cellular and molecular mechanisms that drive these pathogenic transitions remain poorly understood.

Among inflammatory cells, neutrophils are among the first responders to tissue injury and infection. Traditionally viewed as short-lived effector cells of innate immunity, neutrophils are now recognized as highly versatile and plastic cells whose functions extend far beyond host defense. However, their roles in chronic inflammation, tissue remodeling, fibrosis, cancer, and aging have only recently emerged as critical areas of investigation.

Our research focuses on a specific neutrophil-mediated response: the formation of Neutrophil Extracellular Traps (NETs). NETs are web-like structures composed of decondensed DNA decorated with enzymes and proteases that are released into the extracellular space at sites of inflammation. We examine how NETs and neutrophil-driven inflammation contribute to pathological tissue remodeling across multiple disease contexts, including cancer and fibrotic disorders, which become increasingly prevalent with age.

In cancer, our work investigates how inflammatory cells—focusing on neutrophils and NETs—shape the tumor microenvironment and influence cancer cell behavior, stromal activation, and therapeutic response. More broadly, we explore how neutrophil plasticity governs the balance between protective inflammation and pathogenic outcomes associated with aging, such as chronic inflammation, fibrosis, and tumor promotion.

By uncovering fundamental principles that link inflammation, tissue remodeling, aging, and cancer, our research aims to identify novel biomarkers of disease risk and progression, and to inform therapeutic strategies that target pathogenic inflammatory processes rather than tumor cells alone.

Illustration image

Representative fluorescence microscopy image Neutrophil Extracellular Traps (NETs) in vitro.

Activated neutrophils release web-like extracellular DNA structures decorated with neutrophil-derived proteins, forming NETs that extend into the extracellular space. These structures illustrate the characteristic filamentous morphology of NETs following stimulation.

Representative fluorescence microscopy image of NETs surrounding lung metastasis of breast cancer following chemotherapy.

Neutrophils (red) surrounding metastatic tumor cells in the lung release NETs (green), which form extracellular networks within the metastatic niche after treatment.

Representative fluorescence microscopy image of NETs surrounding tumor cells in vitro.

NETs (green) form extracellular, web-like structures following neutrophil activation and extend toward surrounding tumor cells (red).

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IRCAN has a diverse research teams, tackling a wide range and resolution of topics in ageing and cancer.